Neutrophils
Neutrophil Infiltration
N-Formylmethionine Leucyl-Phenylalanine
Chemotaxis, Leukocyte
Peroxidase
Antigens, CD18
Phagocytosis
Superoxides
Chemotactic Factors
Macrophage-1 Antigen
Interleukin-8
Leukotriene B4
Leukocyte Count
Pancreatic Elastase
Cathepsin G
Chemokine CXCL1
Receptors, Interleukin-8B
Complement C5a
Inflammation
NADPH Oxidase
Cells, Cultured
Chemokine CXCL2
Granulomatous Disease, Chronic
Receptors, Formyl Peptide
Cell Movement
Lipopolysaccharides
L-Selectin
Lung
Tetradecanoylphorbol Acetate
Cell Degranulation
Myeloblastin
Luminescent Measurements
Bronchoalveolar Lavage Fluid
alpha-Defensins
Platelet Activating Factor
Mice, Knockout
Granulocyte Colony-Stimulating Factor
Leukocytes
Tumor Necrosis Factor-alpha
Blood Bactericidal Activity
Antigens, CD11b
Receptors, Interleukin-8A
Receptors, IgG
HL-60 Cells
Flow Cytometry
Chemokines
Lactoferrin
Lipocalins
Granulocyte-Macrophage Colony-Stimulating Factor
Leukocyte Disorders
Chemotaxis
Hypochlorous Acid
Chemokines, CXC
Cytokines
P-Selectin
Eosinophils
Monocytes
Opsonin Proteins
Macrophages
Apoptosis
Granulocytes
Cell Adhesion Molecules
NADH, NADPH Oxidoreductases
Reactive Oxygen Species
Antigens, CD11
Antigens, CD
Disease Models, Animal
Signal Transduction
Intercellular Adhesion Molecule-1
Acute-Phase Proteins
Transendothelial and Transepithelial Migration
Leukocyte Rolling
Complement C5
Antibodies, Antineutrophil Cytoplasmic
Defensins
Matrix Metalloproteinase 8
Cathepsins
Peritonitis
Enzyme Activation
Receptors, Complement
Calcium
N-Formylmethionine
Hydrogen Peroxide
Dose-Response Relationship, Drug
Endothelium, Vascular
Receptors, Leukocyte-Adhesion
Cell Membrane
Cell Aggregation
Monokines
Cell Migration Assays, Leukocyte
Nitroblue Tetrazolium
Serine Endopeptidases
E-Selectin
Chemokine CXCL5
Receptors, Leukotriene B4
Immunity, Innate
RNA, Messenger
Cytochrome b Group
Inflammation Mediators
alpha 1-Antitrypsin
Blood Proteins
Peritoneal Cavity
Calgranulin B
Calcimycin
Cytosol
Receptors, Complement 3b
GPI-Linked Proteins
Reperfusion Injury
Receptors, Immunologic
Interleukin-1
Sepsis
Receptor, Anaphylatoxin C5a
Acute Lung Injury
Cell Migration Inhibition
Receptors, Lipoxin
Up-Regulation
Calgranulin A
Hydroxyeicosatetraenoic Acids
Enzyme Inhibitors
Staphylococcus aureus
Antigen-Antibody Complex
Leukocyte-Adhesion Deficiency Syndrome
Receptors, Fc
Arachidonate 5-Lipoxygenase
Immunoglobulin G
Lymphocyte Function-Associated Antigen-1
Skin Window Technique
Molecular Sequence Data
Blood Cell Count
Arthus Reaction
Macrophages, Alveolar
Rabbits
Blood Platelets
Bone Marrow Cells
Lipoxins
Gene Expression Regulation
Enzyme-Linked Immunosorbent Assay
Actins
Antimicrobial Cationic Peptides
Selectins
rac GTP-Binding Proteins
Antibodies
Capillary Permeability
Arachidonic Acid
Bone Marrow
Class Ib Phosphatidylinositol 3-Kinase
Venules
Sputum
Lymphocytes
Endotoxins
Cell Survival
Amino Acid Sequence
Edema
Cattle
Vasculitis
Blotting, Western
Pertussis Toxin
Cell Communication
Receptors, Cell Surface
p38 Mitogen-Activated Protein Kinases
Lung Injury
Protein Kinase C
Bronchoalveolar Lavage
beta-Thromboglobulin
Muramidase
Interleukin-6
Phosphorylation
Mannheimia haemolytica
Matrix Metalloproteinase 9
Exocytosis
Wegener Granulomatosis
Oxidation-Reduction
Complement C5a, des-Arginine
Biological Markers
GM-CSF-deficient mice are susceptible to pulmonary group B streptococcal infection. (1/19639)
Granulocyte-macrophage colony-stimulating factor (GM-CSF) gene-targeted mice (GM-/-) cleared group B streptococcus (GBS) from the lungs more slowly than wild-type mice. Expression of GM-CSF in the respiratory epithelium of GM-/- mice improved bacterial clearance to levels greater than that in wild-type GM+/+ mice. Acute aerosolization of GM-CSF to GM+/+ mice significantly enhanced clearance of GBS at 24 hours. GBS infection was associated with increased neutrophilic infiltration in lungs of GM-/- mice, while macrophage infiltrates predominated in wild-type mice, suggesting an abnormality in macrophage clearance of bacteria in the absence of GM-CSF. While phagocytosis of GBS was unaltered, production of superoxide radicals and hydrogen peroxide was markedly deficient in macrophages from GM-/- mice. Lipid peroxidation, assessed by measuring the isoprostane 8-iso-PGF2alpha, was decreased in the lungs of GM-/- mice. GM-CSF plays an important role in GBS clearance in vivo, mediated in part by its role in enhancing superoxide and hydrogen peroxide production and bacterial killing by alveolar macrophages. (+info)Interaction of inflammatory cells and oral microorganisms. II. Modulation of rabbit polymorphonuclear leukocyte hydrolase release by polysaccharides in response to Streptococcus mutans and Streptococcus sanguis. (2/19639)
The release of lysosomal hydrolases from polymorphonuclear leukocytes (PMNs) has been postulated in the pathogenesis of tissue injury in periodontal disease. In the present study, lysosomal enzyme release was monitored from rabbit peritoneal exudate PMNs exposed to Streptocccus mutans or Streptococcus sanguis. S. mutans grown in brain heart infusion (BHI) broth failed to promote significant PMN enzyme release. S. sanguis grown in BHI broth, although more effective than S. mutants, was a weak stimulus for promotion of PMN hydrolase release. Preincubation of washed, viable S. mutans in sucrose or in different-molecular-weight dextrans resulted in the ability of the organisms to provoke PMN release reactions. This effect could bot be demonstrated with boiled or trypsinized S. mutans or with viable S. sanguis. However, when grown in BHI broth supplemented with sucrose, but not with glucose, both S. mutans and S. sanguis triggered discharge of PMN enzymes. The mechanism(s) whereby dextran or sucrose modulates PMN-bacterial interaction may in some manner be related to promotion of microbial adhesiveness or aggregation by dextran and by bacterial synthesis of glucans from sucrose. (+info)Interaction of inflammatory cells and oral microorganisms. III. Modulation of rabbit polymorphonuclear leukocyte hydrolase release response to Actinomyces viscosus and Streptococcus mutans by immunoglobulins and complement. (3/19639)
In the absence of antiserum, rabbit polymorphonuclear leukocytes (PMNs) released lysosomal enzymes in response to Actinomyces viscosus (19246) but not to Streptococcus mutans (6715). Antibodies had a marked modulating influence on these reactions. PMN hydrolase release was significantly enhanced to both organisms when specific rabbit antiserum and isolated immunoglobulin G (IgG) were included in the incubations. Immune complex F(ab')2 fragments of IgG directed against S. mutans agglutinated bacteria. Immune complexes consisting of S. mutans and F(ab')2 fragments of IgG directed against this organism were not effective as bacteria-IgG complexes in stimulating PMN release. The intensity of the release response to bacteria-IgG complexes was also diminished when PMNs were preincubated with isolated Fc fragments derived from IgG. Fresh serum as a source of complement components had no demonstrable effect on PMN release either alone or in conjuction with antiserum in these experiments. These data may be relevant to the mechanisms and consequences of the interaction of PMNs and plaque bacteria in the pathogenesis of periodontal disease. (+info)Lung weight parallels disease severity in experimental coccidioidomycosis. (4/19639)
Evidence provided by histopathological study of lesions is a valuable adjunct for evaluating chemotherapeutic efficacy in experimental animal models, In addition, this should be correlated with a measure of disease severity in the same animal. The latter could be obtained by homogenization of infected organs and quantitative enumeration of viable cells of the etiological agent, but this would preclude histopathological studies in the same animal. Progression of disease in pulmonary infection is associated with replacement of air space by fluid, cells, and cellular debris. Therefore, an increase in lung weight should reflect severity of disease. Results with the murine model of coccidioidomycosis demonstrate that increasing lung weight parallels the increasing census of fungus cells in the lungs of both treated and nontreated infected mice. This was supported with evidence obtained from microscopic studies of lesions indicating that specific chemotherapy limited spread of the infection and inhibited multiplication of the fungus in the lung. Therefore, lung weight can be used as a measure of disease severity in the murine model of coccidioidomycosis. (+info)Enhanced Th1 activity and development of chronic enterocolitis in mice devoid of Stat3 in macrophages and neutrophils. (5/19639)
We have generated mice with a cell type-specific disruption of the Stat3 gene in macrophages and neutrophils. The mutant mice are highly susceptible to endotoxin shock with increased production of inflammatory cytokines such as TNF alpha, IL-1, IFN gamma, and IL-6. Endotoxin-induced production of inflammatory cytokines is augmented because the suppressive effects of IL-10 on inflammatory cytokine production from macrophages and neutrophils are completely abolished. The mice show a polarized immune response toward the Th1 type and develop chronic enterocolitis with age. Taken together, Stat3 plays a critical role in deactivation of macrophages and neutrophils mainly exerted by IL-10. (+info)Characterization and partial purification of a novel neutrophil membrane-associated kinase capable of phosphorylating the respiratory burst component p47phox. (6/19639)
The phosphorylation of p47phox is widely viewed as an important step in the activation of the neutrophil respiratory burst oxidase system. The exact nature of the kinase(s) responsible remains to be elucidated. We show here that such a kinase was detected on neutrophil membranes activated by either PMA or formyl-methionyl-leucyl-phenylalanine. This enzyme is not intrinsic to the neutrophil membrane and could be eluted with 0.5 M NaCl. The kinase activity was partially purified and was found not to be due to the presence of previously suggested kinases, including protein kinase C isotypes, mitogen-activated protein kinase and protein kinase B. Gel filtration and renaturation in substrate gels suggest a molecular mass of between 45 and 51 kDa. The kinase activity was independent of calcium and lipids but was potently inhibited by staurosporine. Treatment with protein phosphatase 2Ac suggested that the kinase was activated by serine/threonine phosphorylation. Phosphopeptide maps indicated that the kinase phosphorylated p47phox on similar sites to those found in vivo. These results indicate that activation of neutrophils by PMA results in the activation of a membrane-associated kinase that may play a part in the regulation of neutrophil NADPH oxidase through its ability to phosphorylate p47phox. (+info)Non-serum-dependent chemotactic factors produced by Candida albicans stimulate chemotaxis by binding to the formyl peptide receptor on neutrophils and to an unknown receptor on macrophages. (7/19639)
Serum-free culture filtrates of six Candida species and Saccharomyces cerevisiae were found to contain chemoattractants for human polymorphonuclear leukocytes (PMNs) and a mouse macrophage-like cell line, J774. The chemotactic factors differed for the PMN and J774 cells, however, in terms of heat stability, kinetics of liberation by the yeast cells, and divalent cation requirements for production. The chemoattractant in Candida albicans culture filtrates appeared to act through the formyl peptide receptor (FPR) of PMNs, since it was found to induce chemotaxis of Chinese hamster ovary (CHO) cells that were expressing the human FPR but did not induce chemotaxis of wild-type CHO cells. The C. albicans culture filtrates also induced migration of PMNs across confluent monolayers of a human gastrointestinal epithelial cell line, T84; migration occurred in the basolateral-to-apical direction but not the reverse direction, unless the epithelial tight junctions were disrupted. J774 cells did not migrate toward the formylated peptide (fMet-Leu-Phe; fMLF), and chemotaxis toward the C. albicans culture filtrate was not inhibited by an FPR antagonist (t-butoxycarbonyl-Met-Leu-Phe), suggesting that a different receptor mediated J774 cell chemotaxis. In conclusion, we have identified a receptor by which a non-serum-dependent chemotactic factor (NSCF) produced by C. albicans induced chemotaxis of PMNs. Additionally, we have shown that NSCF was active across epithelial monolayers. These findings suggest that NSCFs produced by C. albicans and other yeast species may influence host-pathogen interactions at the gastrointestinal tract mucosal surface by inducing phagocytic-cell infiltration. (+info)Role of the extracellular signal-regulated protein kinase cascade in human neutrophil killing of Staphylococcus aureus and Candida albicans and in migration. (8/19639)
Killing of Staphylococcus aureus and Candida albicans by neutrophils involves adherence of the microorganisms, phagocytosis, and a collaborative action of oxygen reactive species and components of the granules. While a number of intracellular signalling pathways have been proposed to regulate neutrophil responses, the extent to which each pathway contributes to the killing of S. aureus and C. albicans has not been clearly defined. We have therefore examined the effect of blocking one such pathway, the extracellular signal-regulated protein kinase (ERK) cascade, using the specific inhibitor of the mitogen-activated protein kinase/ERK kinase, PD98059, on the ability of human neutrophils to kill S. aureus and C. albicans. Our data demonstrate the presence of ERK2 and a 43-kDa form of ERK but not ERK1 in human neutrophils. Upon stimulation with formyl methionyl leucyl phenylalanine (fMLP), the activities of both ERK2 and the 43-kDa form were stimulated. Despite abrogating the activity of both ERK forms, PD98059 only slightly reduced the ability of neutrophils to kill S. aureus or C. albicans. This is consistent with our finding that PD98059 had no effect on neutrophil adherence or degranulation, although pretreatment of neutrophils with PD98059 inhibited fMLP-stimulated superoxide production by 50%, suggesting that a change in superoxide production per se is not strictly correlated with microbicidal activity. However, fMLP-stimulated chemokinesis was markedly inhibited, while random migration and fMLP-stimulated chemotaxis were partially inhibited, by PD98059. These data demonstrate, for the first time, that the ERK cascade plays only a minor role in the microbicidal activity of neutrophils and that the ERK cascade is involved primarily in regulating neutrophil migration in response to fMLP. (+info)There are several key features of inflammation:
1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.
Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.
There are several types of inflammation, including:
1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.
There are several ways to reduce inflammation, including:
1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.
It's important to note that chronic inflammation can lead to a range of health problems, including:
1. Arthritis
2. Diabetes
3. Heart disease
4. Cancer
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.
Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.
Also known as: chronic granulomatous disease, CGD.
Symptoms of neutropenia may include recurring infections, fever, fatigue, weight loss, and swollen lymph nodes. The diagnosis is typically made through a blood test that measures the number of neutrophils in the blood.
Treatment options for neutropenia depend on the underlying cause but may include antibiotics, supportive care to manage symptoms, and in severe cases, bone marrow transplantation or granulocyte-colony stimulating factor (G-CSF) therapy to increase neutrophil production.
There are several types of leukocyte disorders, including:
1. Leukemia: a malignancy of the blood cells that can affect any type of blood cell, including white blood cells.
2. Neutropenia: a condition characterized by a low number of neutrophils (a type of white blood cell) in the blood.
3. Monocytopenia: a condition characterized by a low number of monocytes (a type of white blood cell) in the blood.
4. Lymphopenia: a condition characterized by a low number of lymphocytes (a type of white blood cell) in the blood.
5. Leukopenia: a condition characterized by a low number of all types of white blood cells in the blood.
6. Thalassemia: a genetic disorder that affects the production of hemoglobin, which is necessary for red blood cells to carry oxygen in the body.
7. Fanconi anemia: a rare genetic disorder that affects the production of white blood cells and increases the risk of cancer and other health problems.
8. Diamond-Blackfan anemia: a rare genetic disorder that affects the production of red blood cells and can also lead to neutropenia and other complications.
9. Chronic granulomatous disease (CGD): a condition caused by a defect in the production of a type of white blood cell called a granulocyte, which makes it difficult for the body to fight off infections.
10. Chediak-Higashi syndrome: a rare genetic disorder that affects the production of white blood cells and increases the risk of infections and other health problems.
Treatment for leukocyte disorders depends on the specific condition and may include medications, blood transfusions, or bone marrow transplantation. In some cases, the only effective treatment is a bone marrow transplant.
Inherited bone marrow failure syndromes (IBMFS) are a group of rare genetic disorders that affect the bone marrow's ability to produce blood cells, including red blood cells, white blood cells, and platelets. These disorders can lead to anemia, neutropenia, thrombocytopenia, and an increased risk of infections and cancer.
The following are some of the most common inherited bone marrow failure syndromes:
1. Fanconi anemia: a rare genetic disorder that affects the production of white blood cells and increases the risk of cancer and other health problems.
2. Diamond-Blackfan anemia: a rare genetic disorder that affects the production of red blood cells and can also lead to neutropenia and other complications.
3. Chronic granulomatous disease (CGD): a condition caused by a defect in the production of a type of white blood cell called a granulocyte, which makes it difficult for the body to fight off infections.
4. Chediak-Higashi syndrome: a rare genetic disorder that affects the production of white blood cells and increases the risk of infection and other health problems.
5. X-linked sideroblastic anemia (XLSA): a rare genetic disorder that affects the production of red blood cells and can also lead to neutropenia and other complications.
6. Leukocyte adhesion deficiency (LAD): a rare genetic disorder that affects the production of white blood cells and increases the risk of infection.
7. Wiskott-Aldrich syndrome: a rare genetic disorder that affects the production of white blood cells and increases the risk of infection and other health problems.
8. X-linked agammaglobulinemia (XLA): a rare genetic disorder that affects the production of antibodies and increases the risk of infections.
9. Common variable immunodeficiency (CVID): a condition caused by a defect in the production of antibodies, which makes it difficult for the body to fight off infections.
10. Ataxia-telangiectasia (AT): a rare genetic disorder that affects the production of immune cells and increases the risk of cancer and other health problems.
It is important to note that these are just a few examples of primary immunodeficiency diseases and there are many more types of disorders that can affect the immune system. Each type of primary immunodeficiency disease has its own set of symptoms and may require different treatments.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
The symptoms of peritonitis can vary depending on the severity and location of the inflammation, but they may include:
* Abdominal pain and tenderness
* Fever
* Nausea and vomiting
* Diarrhea or constipation
* Loss of appetite
* Fatigue
* Weakness
* Low blood pressure
Peritonitis can be diagnosed through a physical examination, medical history, and diagnostic tests such as a CT scan, MRI or ultrasound. Treatment usually involves antibiotics to clear the infection and supportive care to manage symptoms. In severe cases, surgery may be required to remove any infected tissue or repair damaged organs.
Prompt medical attention is essential for effective treatment and prevention of complications such as sepsis, organ failure, and death.
Symptoms of pneumonia may include cough, fever, chills, difficulty breathing, and chest pain. In severe cases, pneumonia can lead to respiratory failure, sepsis, and even death.
There are several types of pneumonia, including:
1. Community-acquired pneumonia (CAP): This type of pneumonia is caused by bacteria or viruses and typically affects healthy people outside of hospitals.
2. Hospital-acquired pneumonia (HAP): This type of pneumonia is caused by bacteria or fungi and typically affects people who are hospitalized for other illnesses or injuries.
3. Aspiration pneumonia: This type of pneumonia is caused by food, liquids, or other foreign matter being inhaled into the lungs.
4. Pneumocystis pneumonia (PCP): This type of pneumonia is caused by a fungus and typically affects people with weakened immune systems, such as those with HIV/AIDS.
5. Viral pneumonia: This type of pneumonia is caused by viruses and can be more common in children and young adults.
Pneumonia is typically diagnosed through a combination of physical examination, medical history, and diagnostic tests such as chest X-rays or blood tests. Treatment may involve antibiotics, oxygen therapy, and supportive care to manage symptoms and help the patient recover. In severe cases, hospitalization may be necessary to provide more intensive care and monitoring.
Prevention of pneumonia includes vaccination against certain types of bacteria and viruses, good hygiene practices such as frequent handwashing, and avoiding close contact with people who are sick. Early detection and treatment can help reduce the risk of complications and improve outcomes for those affected by pneumonia.
This condition can be caused by various factors such as genetic mutations, infections, autoimmune disorders, and certain medications. In severe cases, agranulocytosis can lead to life-threatening infections that require prompt medical treatment.
Some of the common symptoms of agranulocytosis include fever, chills, sore throat, fatigue, and recurring infections. Diagnosis is typically made through blood tests that measure the number and function of white blood cells, including granulocytes. Treatment options for agranulocytosis depend on the underlying cause, but may include antibiotics, antiviral medications, and immunoglobulin replacement therapy in severe cases.
Reperfusion injury can cause inflammation, cell death, and impaired function in the affected tissue or organ. The severity of reperfusion injury can vary depending on the duration and severity of the initial ischemic event, as well as the promptness and effectiveness of treatment to restore blood flow.
Reperfusion injury can be a complicating factor in various medical conditions, including:
1. Myocardial infarction (heart attack): Reperfusion injury can occur when blood flow is restored to the heart muscle after a heart attack, leading to inflammation and cell death.
2. Stroke: Reperfusion injury can occur when blood flow is restored to the brain after an ischemic stroke, leading to inflammation and damage to brain tissue.
3. Organ transplantation: Reperfusion injury can occur when a transplanted organ is subjected to ischemia during harvesting or preservation, and then reperfused with blood.
4. Peripheral arterial disease: Reperfusion injury can occur when blood flow is restored to a previously occluded peripheral artery, leading to inflammation and damage to the affected tissue.
Treatment of reperfusion injury often involves medications to reduce inflammation and oxidative stress, as well as supportive care to manage symptoms and prevent further complications. In some cases, experimental therapies such as stem cell transplantation or gene therapy may be used to promote tissue repair and regeneration.
Here are some key points to define sepsis:
1. Inflammatory response: Sepsis is characterized by an excessive and uncontrolled inflammatory response to an infection. This can lead to tissue damage and organ dysfunction.
2. Systemic symptoms: Patients with sepsis often have systemic symptoms such as fever, chills, rapid heart rate, and confusion. They may also experience nausea, vomiting, and diarrhea.
3. Organ dysfunction: Sepsis can cause dysfunction in multiple organs, including the lungs, kidneys, liver, and heart. This can lead to organ failure and death if not treated promptly.
4. Infection source: Sepsis is usually caused by a bacterial infection, but it can also be caused by fungal or viral infections. The infection can be localized or widespread, and it can affect different parts of the body.
5. Severe sepsis: Severe sepsis is a more severe form of sepsis that is characterized by severe organ dysfunction and a higher risk of death. Patients with severe sepsis may require intensive care unit (ICU) admission and mechanical ventilation.
6. Septic shock: Septic shock is a life-threatening condition that occurs when there is severe circulatory dysfunction due to sepsis. It is characterized by hypotension, vasopressor use, and organ failure.
Early recognition and treatment of sepsis are critical to preventing serious complications and improving outcomes. The Sepsis-3 definition is widely used in clinical practice to diagnose sepsis and severe sepsis.
The symptoms of ALI can vary depending on the severity of the condition, but may include:
* Shortness of breath (dyspnea)
* Chest pain or tightness (pleurisy)
* Cough, which may produce mucus or pus
* Fatigue, confusion, or disorientation
* Low oxygen levels in the blood (hypoxia)
If left untreated, ALI can progress to a more severe condition called acute respiratory distress syndrome (ARDS), which can be fatal. Treatment for ALI typically involves supportive care, such as mechanical ventilation, medications to manage inflammation and fluid buildup in the lungs, and management of underlying causes. In severe cases, extracorporeal membrane oxygenation (ECMO) or lung transplantation may be necessary.
It's important to note that ALI can occur in people of all ages and can be caused by a variety of factors, so it's important to seek medical attention right away if you or someone you know is experiencing symptoms of the condition.
These proteins are essential for white blood cells to stick together and migrate through the blood vessels into tissues, where they can fight off infections. The symptoms of Leukocyte Adhesion Deficiency syndrome vary depending on which gene is mutated and the severity of the mutation.
Some of the common symptoms include recurrent or persistent infections, poor wound healing, delayed development of the skin and mucous membranes, and difficulty fighting off certain types of bacteria, viruses, and fungi. The diagnosis of Leukocyte Adhesion Deficiency syndrome is based on a combination of clinical findings, laboratory tests that measure the function of white blood cells, and genetic analysis that identifies mutations in one of the genes involved in leukocyte adhesion.
Treatment for Leukocyte Adhesion Deficiency syndrome usually involves antibiotics to prevent or treat infections, topical creams or ointments to promote wound healing, and occasionally immunoglobulin replacement therapy to boost the immune system.
Several types of Leukocyte Adhesion Deficiency syndrome exist, each caused by a mutation in a different gene involved in leukocyte adhesion. The most common form of this disorder is called LAMA2 deficiency or Hereditary Angioedema with Giant Lymph Node.
Overall, early diagnosis and appropriate treatment can help manage symptoms and prevent complications associated with Leukocyte Adhesion Deficiency syndrome.
Leukocyte adhesion deficiency (LAD) is a group of rare genetic disorders characterized by impaired leukocyte trafficking and immune dysfunction. The disorders are caused by mutations in genes encoding proteins involved in leukocyte adhesion and migration, such as integrins and chemokine receptors.
There are several types of LAD, each with distinct clinical features and symptoms. The most common form of the disorder is LAMA2 deficiency, which affects approximately 1 in 50,000 individuals worldwide. Other forms of LAD include CD1a and CD1b deficiencies, which are less common but can have overlapping clinical features with LAMA2 deficiency.
The primary symptom of LAD is recurrent skin infections, particularly in childhood. Patients may also experience respiratory infections, gastrointestinal infections, and abscesses. In addition, some patients with LAD may develop chronic inflammation and fibrosis, which can lead to severe complications such as renal failure or blindness.
The diagnosis of LAD is based on a combination of clinical findings, laboratory tests, and genetic analysis. Laboratory tests may include flow cytometry, which can assess leukocyte function and adhesion properties, and molecular genetic testing, which can identify mutations in genes encoding integrins or other adhesion molecules.
Treatment of LAD typically involves antibiotics for recurrent skin and soft tissue infections, as well as management of any underlying chronic inflammation or fibrosis. In some cases, bone marrow transplantation may be considered as a curative therapy.
Overall, LAD is a rare and complex disorder that requires careful diagnosis and management by a multidisciplinary team of healthcare professionals. With appropriate treatment, many patients with LAD can lead active and productive lives, although some may experience ongoing complications or lifelong immune dysfunction.
The Arthus reaction is named after French physician Louis-Jean-Baptiste Arthus, who first described the phenomenon in 1890. It is commonly seen in conditions such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and other autoimmune disorders.
The reaction occurs when antibodies bind to antigens, such as proteins or cells, on the surface of tissues. The binding of antibodies to antigens can activate complement proteins, which are a group of proteins that work together to destroy pathogens. In the case of the Arthus reaction, the activation of complement proteins leads to the formation of a membrane attack complex (MAC), which is composed of various proteins and can cause damage to tissues.
The Arthus reaction can cause a range of symptoms, including joint pain, swelling, and warmth, as well as fever and fatigue. In severe cases, it can lead to permanent joint damage and disability. Treatment options for the Arthus reaction include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and immunosuppressive medications.
In summary, the Arthus reaction is an allergic response that occurs when antibodies bind to antigens and form immune complexes, leading to inflammation and tissue damage. It is commonly seen in autoimmune disorders such as systemic lupus erythematosus and rheumatoid arthritis, and can cause a range of symptoms including joint pain and swelling, fever, and fatigue. Treatment options include NSAIDs, corticosteroids, and immunosuppressive medications.
The most common bacteria that cause pneumonia are Streptococcus pneumoniae (also known as pneumococcus), Haemophilus influenzae, and Staphylococcus aureus. These bacteria can infect the lungs through various routes, including respiratory droplets, contaminated food or water, or direct contact with an infected person.
Symptoms of pneumonia may include cough, fever, chills, shortness of breath, and chest pain. In severe cases, pneumonia can lead to serious complications such as respiratory failure, sepsis, and death.
Diagnosis of pneumonia typically involves a physical examination, medical history, and diagnostic tests such as chest X-rays or blood cultures. Treatment typically involves antibiotics to eliminate the infection, as well as supportive care to manage symptoms and prevent complications. Vaccines are also available to protect against certain types of bacterial pneumonia, particularly in children and older adults.
Preventative measures for bacterial pneumonia include:
* Getting vaccinated against Streptococcus pneumoniae and Haemophilus influenzae type b (Hib)
* Practicing good hygiene, such as washing hands regularly and covering the mouth and nose when coughing or sneezing
* Avoiding close contact with people who are sick
* Staying hydrated and getting enough rest
* Quitting smoking, if applicable
* Managing underlying medical conditions, such as diabetes or heart disease
It is important to seek medical attention promptly if symptoms of pneumonia develop, particularly in high-risk populations. Early diagnosis and treatment can help prevent serious complications and improve outcomes for patients with bacterial pneumonia.
White blood cells are an important part of the immune system and play a crucial role in fighting off infections and diseases. However, when there is an excessive increase in their numbers, it can lead to various complications, including:
1. Increased risk of infection: With too many white blood cells in the bloodstream, there is a higher chance of developing infections.
2. Inflammation: Excessive production of white blood cells can cause inflammation in various parts of the body.
3. Blood clotting disorders: White blood cells can clump together and form clots, which can lead to blockages in blood vessels.
4. Tissue damage: The excessive growth of white blood cells can cause damage to tissues and organs.
5. Bone marrow failure: Prolonged leukocytosis can lead to bone marrow failure, which can result in a decrease in the production of other blood cells, such as red blood cells and platelets.
There are several types of leukocytosis, including:
1. Reactive leukocytosis: This is the most common type and is caused by an infection or inflammation.
2. Chronic leukocytosis: This type is characterized by a persistent increase in white blood cells over a long period of time.
3. Acute leukocytosis: This type is characterized by a sudden and severe increase in white blood cells, often accompanied by other symptoms such as fever and fatigue.
4. Leukemia: This is a type of cancer that affects the bone marrow and blood cells. It can cause an abnormal increase in white blood cells.
Diagnosis of leukocytosis typically involves a physical examination, medical history, and laboratory tests such as complete blood count (CBC) and bone marrow biopsy. Treatment depends on the underlying cause and may include antibiotics for infections, steroids to reduce inflammation, or chemotherapy for leukemia. In some cases, no treatment is necessary if the condition resolves on its own.
There are several types of edema, including:
1. Pitting edema: This type of edema occurs when the fluid accumulates in the tissues and leaves a pit or depression when it is pressed. It is commonly seen in the skin of the lower legs and feet.
2. Non-pitting edema: This type of edema does not leave a pit or depression when pressed. It is often seen in the face, hands, and arms.
3. Cytedema: This type of edema is caused by an accumulation of fluid in the tissues of the limbs, particularly in the hands and feet.
4. Edema nervorum: This type of edema affects the nerves and can cause pain, numbness, and tingling in the affected area.
5. Lymphedema: This is a condition where the lymphatic system is unable to properly drain fluid from the body, leading to swelling in the arms or legs.
Edema can be diagnosed through physical examination, medical history, and diagnostic tests such as imaging studies and blood tests. Treatment options for edema depend on the underlying cause, but may include medications, lifestyle changes, and compression garments. In some cases, surgery or other interventions may be necessary to remove excess fluid or tissue.
There are several types of vasculitis, each with its own set of symptoms and characteristics. Some common forms of vasculitis include:
1. Giant cell arteritis: This is the most common form of vasculitis, and it affects the large arteries in the head, neck, and arms. Symptoms include fever, fatigue, muscle aches, and loss of appetite.
2. Takayasu arteritis: This type of vasculitis affects the aorta and its major branches, leading to inflammation in the blood vessels that supply the heart, brain, and other vital organs. Symptoms include fever, fatigue, chest pain, and shortness of breath.
3. Polymyalgia rheumatica: This is an inflammatory condition that affects the muscles and joints, as well as the blood vessels. It often occurs in people over the age of 50 and is frequently associated with giant cell arteritis. Symptoms include pain and stiffness in the shoulders, hips, and other joints, as well as fatigue and fever.
4. Kawasaki disease: This is a rare condition that affects children under the age of 5, causing inflammation in the blood vessels that supply the heart and other organs. Symptoms include high fever, rash, swollen lymph nodes, and irritability.
The exact cause of vasculitis is not fully understood, but it is thought to be an autoimmune disorder, meaning that the body's immune system mistakenly attacks its own blood vessels. Genetic factors may also play a role in some cases.
Diagnosis of vasculitis typically involves a combination of physical examination, medical history, and diagnostic tests such as blood tests, imaging studies (e.g., MRI or CT scans), and biopsies. Treatment options vary depending on the specific type of vasculitis and its severity, but may include medications to reduce inflammation and suppress the immune system, as well as lifestyle modifications such as exercise and stress management techniques. In severe cases, surgery or organ transplantation may be necessary.
In addition to these specific types of vasculitis, there are other conditions that can cause similar symptoms and may be included in the differential diagnosis, such as:
1. Rheumatoid arthritis (RA): This is a chronic autoimmune disorder that affects the joints and can cause inflammation in blood vessels.
2. Systemic lupus erythematosus (SLE): This is another autoimmune disorder that can affect multiple systems, including the skin, joints, and blood vessels.
3. Polyarteritis nodosa: This is a condition that causes inflammation of the blood vessels, often in association with hepatitis B or C infection.
4. Takayasu arteritis: This is a rare condition that affects the aorta and its branches, causing inflammation and narrowing of the blood vessels.
5. Giant cell arteritis: This is a condition that causes inflammation of the large and medium-sized blood vessels, often in association with polymyalgia rheumatica (PMR).
6. Kawasaki disease: This is a rare condition that affects children, causing inflammation of the blood vessels and potential heart complications.
7. Henoch-Schönlein purpura: This is a rare condition that causes inflammation of the blood vessels in the skin, joints, and gastrointestinal tract.
8. IgG4-related disease: This is a condition that can affect various organs, including the pancreas, bile ducts, and blood vessels, causing inflammation and potentially leading to fibrosis or tumor formation.
It is important to note that these conditions may have similar symptoms and signs as vasculitis, but they are distinct entities with different causes and treatment approaches. A thorough diagnostic evaluation, including laboratory tests and imaging studies, is essential to determine the specific diagnosis and develop an appropriate treatment plan.
Examples of acute diseases include:
1. Common cold and flu
2. Pneumonia and bronchitis
3. Appendicitis and other abdominal emergencies
4. Heart attacks and strokes
5. Asthma attacks and allergic reactions
6. Skin infections and cellulitis
7. Urinary tract infections
8. Sinusitis and meningitis
9. Gastroenteritis and food poisoning
10. Sprains, strains, and fractures.
Acute diseases can be treated effectively with antibiotics, medications, or other therapies. However, if left untreated, they can lead to chronic conditions or complications that may require long-term care. Therefore, it is important to seek medical attention promptly if symptoms persist or worsen over time.
1. Acute respiratory distress syndrome (ARDS): This is a severe and life-threatening condition that occurs when the lungs become inflamed and fill with fluid, making it difficult to breathe.
2. Pneumonia: This is an infection of the lungs that can cause inflammation and damage to the air sacs and lung tissue.
3. Aspiration pneumonitis: This occurs when food, liquid, or other foreign substances are inhaled into the lungs, causing inflammation and damage.
4. Chemical pneumonitis: This is caused by exposure to harmful chemicals or toxins that can damage the lungs and cause inflammation.
5. Radiation pneumonitis: This occurs when the lungs are exposed to high levels of radiation, causing damage and inflammation.
6. Lung fibrosis: This is a chronic condition in which the lungs become scarred and stiff, making it difficult to breathe.
7. Pulmonary embolism: This occurs when a blood clot forms in the lungs, blocking the flow of blood and oxygen to the heart and other organs.
Symptoms of lung injury can include:
* Shortness of breath
* Chest pain or tightness
* Coughing up blood or pus
* Fever
* Confusion or disorientation
Treatment for lung injury depends on the underlying cause and severity of the condition, and may include oxygen therapy, medications to reduce inflammation, antibiotics for infections, and mechanical ventilation in severe cases. In some cases, lung injury can be a life-threatening condition and may require hospitalization and intensive care.
The hallmark of Wegener Granulomatosis is the formation of granulomas, which are clusters of immune cells that form in response to infection or inflammation. In this condition, however, the granulomas are not caused by an infectious agent but rather by the body's own immune system attacking its own tissues.
The symptoms of Wegener Granulomatosis can vary depending on the organs affected and can include:
* Fever
* Joint pain
* Fatigue
* Weight loss
* Shortness of breath
* Chest pain
* Coughing up blood
* Abdominal pain
* Blood in urine or stool
* Headache
The exact cause of Wegener Granulomatosis is not known, but it is believed to involve a combination of genetic and environmental factors. Treatment typically involves the use of corticosteroids and other immunosuppressive medications to reduce inflammation and prevent further damage to the body. In some cases, plasmapheresis (plasma exchange) may also be used to remove harmful antibodies from the blood.
Wegener Granulomatosis is a relatively rare condition, affecting approximately 2-4 people per million each year. It can occur at any age but is most commonly diagnosed in adults between the ages of 40 and 60. With early diagnosis and proper treatment, many people with Wegener Granulomatosis can experience a good outcome and improved quality of life. However, if left untreated, the condition can be fatal.
Some common examples of bacterial infections include:
1. Urinary tract infections (UTIs)
2. Respiratory infections such as pneumonia and bronchitis
3. Skin infections such as cellulitis and abscesses
4. Bone and joint infections such as osteomyelitis
5. Infected wounds or burns
6. Sexually transmitted infections (STIs) such as chlamydia and gonorrhea
7. Food poisoning caused by bacteria such as salmonella and E. coli.
In severe cases, bacterial infections can lead to life-threatening complications such as sepsis or blood poisoning. It is important to seek medical attention if symptoms persist or worsen over time. Proper diagnosis and treatment can help prevent these complications and ensure a full recovery.
Phagocyte bactericidal dysfunction can be caused by a variety of factors, including genetic mutations, exposure to toxins, or infections with certain viruses or other pathogens that interfere with phagocyte function.
The consequences of phagocyte bactericidal dysfunction can include increased susceptibility to infections and the development of persistent or chronic infections, which can lead to a range of health problems and diseases.
Phagocyte bactericidal dysfunction is an important area of research in immunology and infectious disease, as understanding the mechanisms that control phagocyte function can help us develop new therapies and treatments for infections and other immune-related disorders.
Some common types of lung diseases include:
1. Asthma: A chronic condition characterized by inflammation and narrowing of the airways, leading to wheezing, coughing, and shortness of breath.
2. Chronic Obstructive Pulmonary Disease (COPD): A progressive condition that causes chronic inflammation and damage to the airways and lungs, making it difficult to breathe.
3. Pneumonia: An infection of the lungs that can be caused by bacteria, viruses, or fungi, leading to fever, chills, coughing, and difficulty breathing.
4. Bronchiectasis: A condition where the airways are damaged and widened, leading to chronic infections and inflammation.
5. Pulmonary Fibrosis: A condition where the lungs become scarred and stiff, making it difficult to breathe.
6. Lung Cancer: A malignant tumor that develops in the lungs, often caused by smoking or exposure to carcinogens.
7. Cystic Fibrosis: A genetic disorder that affects the respiratory and digestive systems, leading to chronic infections and inflammation in the lungs.
8. Tuberculosis (TB): An infectious disease caused by Mycobacterium Tuberculosis, which primarily affects the lungs but can also affect other parts of the body.
9. Pulmonary Embolism: A blockage in one of the arteries in the lungs, often caused by a blood clot that has traveled from another part of the body.
10. Sarcoidosis: An inflammatory disease that affects various organs in the body, including the lungs, leading to the formation of granulomas and scarring.
These are just a few examples of conditions that can affect the lungs and respiratory system. It's important to note that many of these conditions can be treated with medication, therapy, or surgery, but early detection is key to successful treatment outcomes.
In adults, RDS is less common than in newborns but can still occur in certain situations. These include:
* Sepsis (a severe infection that can cause inflammation throughout the body)
* Pneumonia or other respiratory infections
* Injury to the lung tissue, such as from a car accident or smoke inhalation
* Burns that cover a large portion of the body
* Certain medications, such as those used to treat cancer or autoimmune disorders.
Symptoms of RDS in adults can include:
* Shortness of breath
* Rapid breathing
* Chest tightness or pain
* Low oxygen levels in the blood
* Blue-tinged skin (cyanosis)
* Confusion or disorientation
Diagnosis of RDS in adults is typically made based on a combination of physical examination, medical history, and diagnostic tests such as chest X-rays or blood gas analysis. Treatment may involve oxygen therapy, mechanical ventilation (a machine that helps the patient breathe), and medications to help increase surfactant production or reduce inflammation in the lungs. In severe cases, a lung transplant may be necessary.
Prevention of RDS in adults includes avoiding exposure to risk factors such as smoking and other pollutants, maintaining good overall health, and seeking prompt medical attention if any respiratory symptoms develop.
The primary symptom of CHS is a weakened immune system, which makes patients more susceptible to infections such as pneumonia and meningitis. Other common symptoms include:
* Easy bruising and bleeding
* Poor wound healing
* Recurring skin rashes
* Enlarged lymph nodes
* Joint pain and stiffness
* Vision loss or blindness
There is no cure for CHS, but bone marrow transplantation has been shown to be effective in improving the immune system and reducing the risk of complications. Treatment also includes antibiotics to prevent and treat infections, as well as other supportive therapies to manage symptoms such as joint pain and vision loss.
The prognosis for CHS is generally poor, with many patients dying before the age of 20 due to complications related to infection or organ failure. However, with early diagnosis and appropriate treatment, some patients have been able to survive into adulthood.
CHS is an autosomal recessive disorder, meaning that it is caused by mutations in both copies of the CHS1 gene. This means that children must inherit one mutated copy of the gene from each parent in order to develop the condition.
There are several other conditions that can cause similar symptoms to CHS, including:
* X-linked severe combined immunodeficiency (XSCID)
* Leukocyte adhesion deficiency (LAD)
* Chronic granulomatous disease (CGD)
It is important for healthcare providers to be aware of these conditions and to consider them in the differential diagnosis when evaluating patients with symptoms similar to those of CHS.
Endotoxemia can occur in individuals who have a severe bacterial infection, such as pneumonia or meningitis, or those who have a prosthetic device or other foreign body that becomes infected with gram-negative bacteria. Treatment of endotoxemia typically involves antibiotics and supportive care to manage symptoms and prevent further complications. In severe cases, medications such as corticosteroids and vasopressors may be used to help reduce inflammation and improve blood flow.
Endotoxemia is a serious medical condition that requires prompt diagnosis and treatment to prevent complications and improve outcomes for patients.
Symptoms of cystic fibrosis can vary from person to person, but may include:
* Persistent coughing and wheezing
* Thick, sticky mucus that clogs airways and can lead to respiratory infections
* Difficulty gaining weight or growing at the expected rate
* Intestinal blockages or digestive problems
* Fatty stools
* Nausea and vomiting
* Diarrhea
* Rectal prolapse
* Increased risk of liver disease and respiratory failure
Cystic fibrosis is usually diagnosed in infancy, and treatment typically includes a combination of medications, respiratory therapy, and other supportive care. Management of the disease focuses on controlling symptoms, preventing complications, and improving quality of life. With proper treatment and care, many people with cystic fibrosis can lead long, fulfilling lives.
In summary, cystic fibrosis is a genetic disorder that affects the respiratory, digestive, and reproductive systems, causing thick and sticky mucus to build up in these organs, leading to serious health problems. It can be diagnosed in infancy and managed with a combination of medications, respiratory therapy, and other supportive care.
Pseudomonas infections are challenging to treat due to the bacteria's ability to develop resistance against antibiotics. The treatment typically involves a combination of antibiotics and other supportive therapies, such as oxygen therapy or mechanical ventilation, to manage symptoms and prevent complications. In some cases, surgical intervention may be necessary to remove infected tissue or repair damaged organs.
There are several types of dermatitis, including:
1. Atopic dermatitis: a chronic condition characterized by dry, itchy skin and a tendency to develop allergies.
2. Contact dermatitis: a localized reaction to an allergen or irritant that comes into contact with the skin.
3. Seborrheic dermatitis: a condition characterized by redness, itching, and flaking skin on the scalp, face, or body.
4. Psoriasis: a chronic condition characterized by thick, scaly patches on the skin.
5. Cutaneous lupus erythematosus: a chronic autoimmune disorder that can cause skin rashes and lesions.
6. Dermatitis herpetiformis: a rare condition characterized by itchy blisters or rashes on the skin.
Dermatitis can be diagnosed through a physical examination, medical history, and sometimes laboratory tests such as patch testing or biopsy. Treatment options for dermatitis depend on the cause and severity of the condition, but may include topical creams or ointments, oral medications, phototherapy, or lifestyle changes such as avoiding allergens or irritants.
Symptoms of pulmonary edema may include:
* Shortness of breath (dyspnea)
* Coughing up frothy sputum
* Chest pain or tightness
* Fatigue
* Confusion or disorientation
Pulmonary edema can be diagnosed through physical examination, chest x-rays, electrocardiogram (ECG), and blood tests. Treatment options include oxygen therapy, diuretics, and medications to manage underlying conditions such as heart failure or sepsis. In severe cases, hospitalization may be necessary to provide mechanical ventilation.
Prevention measures for pulmonary edema include managing underlying medical conditions, avoiding exposure to pollutants and allergens, and seeking prompt medical attention if symptoms persist or worsen over time.
In summary, pulmonary edema is a serious condition that can impair lung function and lead to shortness of breath, chest pain, and other respiratory symptoms. Prompt diagnosis and treatment are essential to prevent complications and improve outcomes for patients with this condition.
Necrosis is a type of cell death that occurs when cells are exposed to excessive stress, injury, or inflammation, leading to damage to the cell membrane and the release of cellular contents into the surrounding tissue. This can lead to the formation of gangrene, which is the death of body tissue due to lack of blood supply.
There are several types of necrosis, including:
1. Coagulative necrosis: This type of necrosis occurs when there is a lack of blood supply to the tissues, leading to the formation of a firm, white plaque on the surface of the affected area.
2. Liquefactive necrosis: This type of necrosis occurs when there is an infection or inflammation that causes the death of cells and the formation of pus.
3. Caseous necrosis: This type of necrosis occurs when there is a chronic infection, such as tuberculosis, and the affected tissue becomes soft and cheese-like.
4. Fat necrosis: This type of necrosis occurs when there is trauma to fatty tissue, leading to the formation of firm, yellowish nodules.
5. Necrotizing fasciitis: This is a severe and life-threatening form of necrosis that affects the skin and underlying tissues, often as a result of bacterial infection.
The diagnosis of necrosis is typically made through a combination of physical examination, imaging studies such as X-rays or CT scans, and laboratory tests such as biopsy. Treatment depends on the underlying cause of the necrosis and may include antibiotics, surgical debridement, or amputation in severe cases.
Also known as: Corneal inflammation, Eye inflammation, Keratoconjunctivitis, Ocular inflammation.
The symptoms of hemorrhagic shock may include:
* Pale, cool, or clammy skin
* Fast heart rate
* Shallow breathing
* Confusion or loss of consciousness
* Decreased urine output
Treatment of hemorrhagic shock typically involves replacing lost blood volume with IV fluids and/or blood transfusions. In severe cases, medications such as vasopressors may be used to raise blood pressure and improve circulation. Surgical intervention may also be necessary to control the bleeding source.
The goal of treatment is to restore blood flow and oxygenation to vital organs, such as the brain, heart, and kidneys, and to prevent further bleeding and hypovolemia. Early recognition and aggressive treatment of hemorrhagic shock are critical to preventing severe complications and mortality.
There are several symptoms of RA, including:
1. Joint pain and stiffness, especially in the hands and feet
2. Swollen and warm joints
3. Redness and tenderness in the affected areas
4. Fatigue, fever, and loss of appetite
5. Loss of range of motion in the affected joints
6. Firm bumps of tissue under the skin (rheumatoid nodules)
RA can be diagnosed through a combination of physical examination, medical history, blood tests, and imaging studies such as X-rays or ultrasound. Treatment typically involves a combination of medications, including nonsteroidal anti-inflammatory drugs (NSAIDs), disease-modifying anti-rheumatic drugs (DMARDs), and biologic agents. Lifestyle modifications such as exercise and physical therapy can also be helpful in managing symptoms and improving quality of life.
There is no cure for RA, but early diagnosis and aggressive treatment can help to slow the progression of the disease and reduce symptoms. With proper management, many people with RA are able to lead active and fulfilling lives.
Neutrophil
Neutrophil collagenase
Neutrophil swarming
Hypersegmented neutrophil
Neutrophil elastase
Neutrophil oxidative index
Absolute neutrophil count
Neutrophil immunodeficiency syndrome
Neutrophil extracellular traps
Neutrophil cytosolic factor 4
Neutrophil-specific granule deficiency
Neutrophil cytosolic factor 2
Anti-neutrophil cytoplasmic antibody
Neutrophil to lymphocyte ratio
Neutrophil cytosolic factor 1
Nonspecific immune cell
Tumor-infiltrating lymphocytes
Vaginal cytology
Siglec
Oxidative stress
C5a receptor
MMP3
Edgar Pick
Neutrophilia
White blood cell
CCL3
Proteinase 3
Stomatitis nicotina
Granulomatous meningoencephalitis
Clonal hypereosinophilia
Neutrophils: MedlinePlus Medical Encyclopedia Image
Comprehensive characterization of neutrophil genome topology | bioRxiv
Emphysema: Novel Neutrophil Elastase Isoform Discovered | RT
Glucose homeostasis in relation to neutrophil mobilization | COPD
Salmeterol with fluticasone enhances the suppression of IL-8 release and increases the translocation of glucocorticoid receptor...
Absolute Neutrophil Count (ANC)
Platelets Amplify Neutrophil Polarization Induced by the Thromboxane Mimetic U46619 | Clinical Science | Portland Press
Neutrophil Elastase (NEG), Human | LeeBio.com
Role of the Neutrophil NADPH Oxidase and S100A8/A9 in the Pathophysiology of Chronic Inflammation | IntechOpen
Linker histone H1.2 and H1.4 affect the neutrophil lineage determination | eLife
Braz J Med Biol Res - Metabolic fate of glutamine in lymphocytes, macrophages and neutrophils
Frontiers | Systems Immunology Analysis Reveals an Immunomodulatory Effect of Snail-p53 Binding on Neutrophil- and T Cell...
Neutrophil extracellular trap-associated carbamylation and histones trigger osteoclast formation in rheumatoid arthritis |...
Role of p190RhoGAP in beta(2) integrin regulation of RhoA in human neutrophils | Lund University Publications
WHO EMRO | Role of neutrophils in cutaneous leishmaniasis | Volume 16, issue 10 | EMHJ volume 16, 2010
Rat NE/ELA2 (Neutrophil Elastase/Elastase-2) ELISA Kit | G-EC-05121 | Gentaur Elisa Kits
Neutrophils in Resistance to Experimental Infection | Soligenix
The interplay between Pseudomonas aeruginosa and human macrophages and neutrophils - Nottingham ePrints
Reduction in White Blood Cell, Neutrophil, and Red Blood Cell Counts Related to Sex, HLA, and Islet Autoantibodies in Swedish...
The EGFR/ErbB inhibitor neratinib modifies the neutrophil phosphoproteome and promotes apoptosis and clearance by airway...
Neutrophil Trogocytosis blocked by Ancell anti-CD18 mAb and F(ab')2 reagents in a CD47-SIRPa checkpoint disrupted model -...
neutrophil tcells | Immunopaedia
NHANES 1999-2000:
Complete Blood Count with 5-part Differential - Whole Blood Data Documentation, Codebook, and...
N2018 Organization | The Neutrophil
RARECARE.WORLD\Neutrophils in blood ActivityDefinition - FHIR v4.0.1
Therapeutic laser and inflammatory cells - part 2: neutrophils
Molecular regulation of neutrophil responses in inflammation - Nuffield Department of Orthopaedics, Rheumatology and...
Nature Reviews Immunology
Bahrain Medical Laboratory | Cytoplasmic Neutrophil Antibodies, Serum
Origins and unconventional behavior of neutrophils in developing zebrafish - Institut Pasteur
Elastase7
- In addition, we quantified neutrophil elastase (ELISA) and net proteinase activity (substrate assay) in BALF. (dovepress.com)
- We observed no corresponding correlations for neutrophil elastase, net proteinase or gelatinase activity. (dovepress.com)
- Lee Biosolutions is the leading producer of human neutrophil Elastase (ELA2) for clinical research, life science and diagnostic manufacturing uses. (leebio.com)
- The neutrophil form of elastase is 218 amino acids long, with two asparagine-linked carbohydrate chains. (leebio.com)
- Current studies show that both Cathepsin G and Neutrophil Elastase are key enzymes for tissue injury caused by activated neutrophils, such as occurs in Acute Lung injury. (leebio.com)
- One study with C57BL/6 mice demonstrated that the interaction of L. major-infected macrophages with dying neutrophils induced parasite destruction mediated by neutrophil elastase and tumour necrosis factor-α production from neutrophils [5]. (who.int)
- NET-mediated osteoclastogenesis appears to depend on Toll-like receptor 4 signalling and NET-associated proteins including histones and neutrophil elastase. (bmj.com)
Macrophages and neutrophils4
- This amino acid has been shown to play a role in lymphocyte proliferation, cytokine production by lymphocytes and macrophages and phagocytosis and superoxide production by macrophages and neutrophils. (who.int)
- Lymphocytes, macrophages and neutrophils play an important role in the immune and inflammatory response. (who.int)
- The metabolic fate of glutamine in lymphocytes, macrophages and neutrophils will be discussed in the present paper. (who.int)
- For instance, the tumor microenvironment modulates the immune response by selectively attracting and repolarizing immune cells (e.g. macrophages and neutrophils) from an anti-tumorigenic to a pro-tumorigenic phenotype ( 2 , 3 ). (frontiersin.org)
Extracellular2
- The three best described defense mechanisms of neutrophils are phagocytosis (engulfment of pathogenic microorganisms and subsequent destruction in phagosomes), degranulation (the release of antimicrobial proteins from granules to the extracellular space) and the formation of neutrophil extracellular traps (NETs). (elifesciences.org)
- Carbamylation is a posttranslational modification linked to increased bone erosion in RA and we previously showed that carbamylation is present in RA neutrophil extracellular traps (NETs). (bmj.com)
Cytokines1
- The neutrophil-related cytokines IL-36α, -β and -γ were quantified (ELISA) along with IL-6, IL-8, INF-γ and CXCL10 (U-Plex ® ) in plasma and cell-free BAL fluid (BALF). (dovepress.com)
Pathogens2
- Neutrophils are important innate immune cells that tackle invading pathogens with different effector mechanisms. (elifesciences.org)
- NETs are chromatin structures studded with antimicrobial proteins derived mostly from neutrophil granules, which can trap pathogens ( Papayannopoulos, 2018 ). (elifesciences.org)
Inflammatory1
- In homeostatic conditions, up to 2 × 10 11 neutrophils enter the blood stream per day and patrol the host's body until they sense signs of infection, which triggers them to leave the blood stream and migrate to the inflammatory site where they ensure pathogen removal. (elifesciences.org)
Assay3
- Description: A sandwich quantitative ELISA assay kit for detection of Human Defensin Alpha 1, Neutrophil (DEFa1) in samples from serum, plasma, tissue homogenates, cell lysates, cell culture supernates or other biological fluids. (lipidx.org)
- Description: This is Double-antibody Sandwich Enzyme-linked immunosorbent assay for detection of Mouse Defensin Alpha 1, Neutrophil (DEFa1) in serum, plasma, tissue homogenates and other biological fluids. (lipidx.org)
- Description: Enzyme-linked immunosorbent assay based on the Double-antibody Sandwich method for detection of Mouse Defensin Alpha 1, Neutrophil (DEFa1) in samples from serum, plasma, tissue homogenates and other biological fluids with no significant corss-reactivity with analogues from other species. (lipidx.org)
Eosinophils1
- One of these differentiation programs, called granulopoiesis, leads to the development of granulocytes - basophils, eosinophils and neutrophils. (elifesciences.org)
Neutrophilic2
- Large numbers of immature forms of neutrophils, called neutrophilic band cells, are produced by the bone marrow when the demand is high. (medlineplus.gov)
- Neutrophils, also known as neutrophilic polymorphonuclear leukocytes, are the major class of white blood cell in human peripheral blood. (leebio.com)
Polymorphonuclear1
- Polymorphonuclear (PMN) neutrophils have been reported to have a crucial role in the destruction of the Leishmania major parasites at an early stage of infection [2,3]. (who.int)
Phagocytosis1
- Microscope images confirmed that neutrophils appeared to have an important role in leishmania elimination through phagocytosis of amastigotes in the later stages of the disease process. (who.int)
Abstract2
- ABSTRACT Neutrophils are always present in the cytomorphologic process of leishmaniasis but their role is still not fully understood. (who.int)
- article{18081955-679d-4f8b-aa8b-27b69763024d, abstract = {{We found that engagement of beta (2) integrins on human neutrophils induced activation of RhoA, as indicated by the increased ratio of GTP:GTP + GDP recovered on RhoA and translocation of RhoA to a membrane fraction. (lu.se)
ELISA1
- Description: A sandwich ELISA kit for detection of Neutrophil Activating Protein 3 from Mouse in samples from blood, serum, plasma, cell culture fluid and other biological fluids. (novosides.eu)
Systemic1
- In smokers with COPD, altered glucose homeostasis is associated with local and systemic signs of increased neutrophil mobilization, but not with local proteinases. (dovepress.com)
Recruitment1
- Flow cytometric profiling of whole lung lavage (WLL) cells revealed that neutrophil recruitment was the greatest at day 1 and declined to 36.6% of that level in MWCNT- and 16.8% in C60F-treated mice by day 7, and to basal levels by day 28, suggesting a rapid initiation phase and an extended resolution phase. (cdc.gov)
Occurs2
- Under homeostatic conditions, NET formation occurs in mature, circulating neutrophils and therefore we propose that specific cues during neutrophil differentiation shape their ability to form NETs. (elifesciences.org)
- We were surprised to find that the differentiation of these primitive neutrophils occurs only after primitive myeloid progenitors have dispersed in the tissues. (archives-ouvertes.fr)
Destruction1
- However, the mechanisms by which neutrophils participate in bone destruction remain unclear. (bmj.com)
Lung1
- Both ENMs stimulated acute inflammation, predominated by neutrophils, in the lung at day 1, which transitioned to histiocytic inflammation by day 7. (cdc.gov)
Infection1
- Neutrophils are a type of white blood cell that is responsible for much of the body's protection against infection. (medlineplus.gov)
Differentiation3
- Here, we show a critical role for linker histone H1 on the differentiation and function of neutrophils using a genome-wide CRISPR/Cas9 screen in the human cell line PLB-985. (elifesciences.org)
- Loss of H1.2 and H1.4 induced an eosinophil-like transcriptional program, thereby negatively regulating the differentiation into the neutrophil lineage. (elifesciences.org)
- Importantly, H1 subtypes also affect neutrophil differentiation and the eosinophil-directed bias of murine bone marrow stem cells, demonstrating an unexpected subtype-specific role for H1 in granulopoiesis. (elifesciences.org)
COPD3
- Given that these morbidities all display increased neutrophil mobilization, the current study aimed to address whether glucose homeostasis relates to signs of neutrophil mobilization in COPD. (dovepress.com)
- The LTS+COPD group had lower fasting glucose, greater change in glucose during OGTT and higher neutrophil concentrations in BAL and blood compared with HNS. (dovepress.com)
- Fasting glucose correlated in a positive manner with blood neutrophil concentration, forced expiratory volume in 1 second/forced vital capacity ratio (FEV 1 /FVC) and FEV 1 (% of predicted) in LTS+COPD. (dovepress.com)
Immune cells1
- Strikingly, we reveal that IFN-γ is expressed primarily by hepatic neutrophils , not by conventional immune cells with known IFN-γ-producing capability, e.g. (bvsalud.org)
Bone2
- Neutrophils are produced in the bone marrow and released into the bloodstream to travel to wherever they are needed. (medlineplus.gov)
- Objective Neutrophil infiltration into the synovial joint is a hallmark of rheumatoid arthritis (RA), a disease characterised by progressive bone erosion. (bmj.com)
Cells5
- The Absolute Neutrophil Count (ANC) is a calculated parameter based on the total number of white blood cells, the percentage of neutrophils, and the percentage of band cells in a patient's blood sample at a given time. (medscape.com)
- Positivity for multiple IAs showed the lowest counts in white blood cells and neutrophils in boys and red blood cells, hemoglobin, and hematocrit in girls. (arctichealth.org)
- We conclude that the reduction in neutrophils and red blood cells in children with multiple IAs and HLA-DR3-DQ2/DR4-DQ8 genotype may signal a sex-dependent islet autoimmunity detected in longitudinal CBCs. (arctichealth.org)
- The use of Neutrophils from FERMT3 patients elucidated the requirement of kindlen3-CD18 interaction for synapse formation and trogocytosis of antibody opsinized SIRPa-CD47 checkpoint disruped cancer cells in vitro. (ancell.com)
- Dr. Vora] Ted, it's a less common bacteria, which is in the category of what we call Gram- negative bacteria, and it is kind of rather unique because it likes to stay inside a cell and infect the defender cells, which are the neutrophils. (cdc.gov)
Mice1
- After the repetitive exposure, the older mice also had higher numbers of neutrophils in their BAL fluid. (cdc.gov)
Laboratory1
- A recent study from our laboratory has shown that neutrophils also utilize glutamine at high rates (6). (who.int)
Human5
- In this study, the molecular mechanism behind the effectiveness of this combination therapy is investigated in human neutrophils. (springer.com)
- Human neutrophils were preincubated with salmeterol or FP or the combination. (springer.com)
- An efficient neutrophil response is crucial for human antimicrobial defense and, correspondingly, neutropenia is associated with severe infections ( Klein, 2011 ). (elifesciences.org)
- We found that engagement of beta (2) integrins on human neutrophils induced activation of RhoA, as indicated by the increased ratio of GTP:GTP + GDP recovered on RhoA and translocation of RhoA to a membrane fraction. (lu.se)
- This controlled opening and degradation was further carried out in vitro with human neutrophils. (cdc.gov)
Role2
Primarily1
- The white blood cell and neutrophil counts were reduced in children with IAs, primarily in boys. (arctichealth.org)
Blood3
- Neutrophils were quantified in blood and bronchoalveolar lavage samples (BAL). (dovepress.com)
- In this group, the concentration of IL-36α in BALF correlated in a negative manner with fasting glucose, blood neutrophil concentration and FEV 1 , while the CXCL10 concentration in BALF correlated in a negative manner with glucose at the end of OGTT (120 min). (dovepress.com)
- Reduction in White Blood Cell, Neutrophil, and Red Blood Cell Counts Related to Sex, HLA, and Islet Autoantibodies in Swedish TEDDY Children at Increased Risk for Type 1 Diabetes. (arctichealth.org)
Leukocytes2
- Neutrophils constitute 60% of the circulating leukocytes. (who.int)
- Neutrophils are the most abundant leukocytes in humans. (elifesciences.org)
Production2
- Cigarette smoke medium (CSM) induces an increased expression of CXC receptors and the production of ROS that may explain the strong production of IL-8 by neutrophils. (springer.com)
- This leads eventually to suppression of both the NF-κB and MAPK pathways and, hence, to less IL-8 production by the neutrophil. (springer.com)
Injury1
- Neutrophils exacerbate acetaminophen-induced liver injury by producing cytotoxic interferon-γ. (bvsalud.org)
Type1
- By 2 days after fertilization, these neutrophils have become the major leukocyte type found wandering in the epidermis and mesenchyme. (archives-ouvertes.fr)
Found1
- Recently, we have found that neutrophils also utilize glutamine. (who.int)
Kind1
- It kind of subverts the system of neutrophils and takes it over and prevents it from dying and just multiplies. (cdc.gov)
Response1
- Notably, we observed a significant enrichment in transcripts involved in immune response pathways especially those contributing to neutrophil (IL8) and T-cell mediated immunity (BCL6, and CD81). (frontiersin.org)
Patients1
- undertaken from July 15th, 2017 to March 15th, 2018.The multicentrique de cohorte prospective a inclus des Glasgow Coma Scale helped to determine the severety of the patients consécutifs admis en phase aiguë d AVC, disease at admission. (who.int)