COUP Transcription Factor I
COUP Transcription Factor II
COUP Transcription Factors
Bronchoalveolar Lavage Fluid
Passive Cutaneous Anaphylaxis
Disease Models, Animal
Nucleic Acid Hybridization
Bronchial Provocation Tests
Interleukin-8 receptor modulates IgE production and B-cell expansion and trafficking in allergen-induced pulmonary inflammation. (1/4583)We examined the role of the interleukin-8 (IL-8) receptor in a murine model of allergen-induced pulmonary inflammation using mice with a targeted deletion of the murine IL-8 receptor homologue (IL-8r-/-). Wild-type (Wt) and IL-8r-/- mice were systemically immunized to ovalbumin (OVA) and were exposed with either single or multiple challenge of aerosolized phosphate-buffered saline (OVA/PBS) or OVA (OVA/OVA). Analysis of cells recovered from bronchoalveolar lavage (BAL) revealed a diminished recruitment of neutrophils to the airway lumen after single challenge in IL-8r-/- mice compared with Wt mice, whereas multiply challenged IL-8r-/- mice had increased B cells and fewer neutrophils compared with Wt mice. Both Wt and IL-8r-/- OVA/OVA mice recruited similar numbers of eosinophils to the BAL fluid and exhibited comparable degrees of pulmonary inflammation histologically. Both total and OVA-specific IgE levels were greater in multiply challenged IL-8r-/- OVA/OVA mice than in Wt mice. Both the IL-8r-/- OVA/OVA and OVA/PBS mice were significantly less responsive to methacholine than their respective Wt groups, but both Wt and IL-8r mice showed similar degrees of enhancement after multiple allergen challenge. The data demonstrate that the IL-8r modulates IgE production, airway responsiveness, and the composition of the cells (B cells and neutrophils) recruited to the airway lumen in response to antigen. (+info)
Prolonged eosinophil accumulation in allergic lung interstitium of ICAM-2 deficient mice results in extended hyperresponsiveness. (2/4583)ICAM-2-deficient mice exhibit prolonged accumulation of eosinophils in lung interstitium concomitant with a delayed increase in eosinophil numbers in the airway lumen during the development of allergic lung inflammation. The ICAM-2-dependent increased and prolonged accumulation of eosinophils in lung interstitium results in prolonged, heightened airway hyperresponsiveness. These findings reveal an essential role for ICAM-2 in the development of the inflammatory and respiratory components of allergic lung disease. This phenotype is caused by the lack of ICAM-2 expression on non-hematopoietic cells. ICAM-2 deficiency on endothelial cells causes reduced eosinophil transmigration in vitro. ICAM-2 is not essential for lymphocyte homing or the development of leukocytes, with the exception of megakaryocyte progenitors, which are significantly reduced. (+info)
Zonula occludens toxin is a powerful mucosal adjuvant for intranasally delivered antigens. (3/4583)Zonula occludens toxin (Zot) is produced by toxigenic strains of Vibrio cholerae and has the ability to reversibly alter intestinal epithelial tight junctions, allowing the passage of macromolecules through the mucosal barrier. In the present study, we investigated whether Zot could be exploited to deliver soluble antigens through the nasal mucosa for the induction of antigen-specific systemic and mucosal immune responses. Intranasal immunization of mice with ovalbumin (Ova) and recombinant Zot, either fused to the maltose-binding protein (MBP-Zot) or with a hexahistidine tag (His-Zot), induced anti-Ova serum immunoglobulin G (IgG) titers that were approximately 40-fold higher than those induced by immunization with antigen alone. Interestingly, Zot also stimulated high anti-Ova IgA titers in serum, as well as in vaginal and intestinal secretions. A comparison with Escherichia coli heat-labile enterotoxin (LT) revealed that the adjuvant activity of Zot was only sevenfold lower than that of LT. Moreover, Zot and LT induced similar patterns of Ova-specific IgG subclasses. The subtypes IgG1, IgG2a, and IgG2b were all stimulated, with a predominance of IgG1 and IgG2b. In conclusion, our results highlight Zot as a novel potent mucosal adjuvant of microbial origin. (+info)
Anaphylactic bronchoconstriction in BP2 mice: interactions between serotonin and acetylcholine. (4/4583)1. Immunized BP2 mice developed an acute bronchoconstriction in vivo and airway muscle contraction in vitro in response to ovalbumin (OA) and these contractions were dose dependent. 2. Methysergide or atropine inhibited OA-induced bronchoconstriction in vivo and airway muscle contraction in vitro. 3. Neostigmine potentiated the OA-induced bronchoconstriction in vivo and airway muscle contraction in vitro of BP2 mice. This potentiation was markedly reduced by the administration of methysergide or atropine and when the two antagonists were administered together, the responses were completely inhibited. 4. Neostigmine also potentiated the serotonin (5-HT)- and acetylcholine (ACh)-induced bronchoconstriction and this potentiation was significantly reversed by atropine. 5. These results indicate that OA provokes a bronchoconstriction in immunized BP2 mice by stimulating the release of 5-HT, which in turn acts via the cholinergic mediator, ACh. (+info)
Stabilization of L-ascorbic acid by superoxide dismutase and catalase. (5/4583)The effects of superoxide dismutase (SOD) and catalase on the autoxidation rate of L-ascorbic acid (ASA) in the absence of metal ion catalysts were examined. The stabilization of ASA by SOD was confirmed, and the enzyme activity of SOD, which scavenges the superoxide anion formed during the autoxidation of ASA, contributed strongly to this stabilization. The stabilization of ASA by catalase was observed for the first time; however, the specific enzyme ability of catalase would not have been involved in the stabilization of ASA. Such proteins as bovine serum albumin (BSA) and ovalbumin also inhibited the autoxidation of ASA, therefore it seems that non-specific interaction between ASA and such proteins as catalase and BSA might stabilize ASA and that the non-enzymatic superoxide anion scavenging ability of proteins might be involved. (+info)
Contributory and exacerbating roles of gaseous ammonia and organic dust in the etiology of atrophic rhinitis. (6/4583)Pigs reared commercially indoors are exposed to air heavily contaminated with particulate and gaseous pollutants. Epidemiological surveys have shown an association between the levels of these pollutants and the severity of lesions associated with the upper respiratory tract disease of swine atrophic rhinitis. This study investigated the role of aerial pollutants in the etiology of atrophic rhinitis induced by Pasteurella multocida. Forty, 1-week-old Large White piglets were weaned and divided into eight groups designated A to H. The groups were housed in Rochester exposure chambers and continuously exposed to the following pollutants: ovalbumin (groups A and B), ammonia (groups C and D), ovalbumin plus ammonia (groups E and F), and unpolluted air (groups G and H). The concentrations of pollutants used were 20 mg m-3 total mass and 5 mg m-3 respirable mass for ovalbumin dust and 50 ppm for ammonia. One week after exposure commenced, the pigs in groups A, C, E, and G were infected with P. multocida type D by intranasal inoculation. After 4 weeks of exposure to pollutants, the pigs were killed and the extent of turbinate atrophy was assessed with a morphometric index (MI). Control pigs kept in clean air and not inoculated with P. multocida (group H) had normal turbinate morphology with a mean MI of 41.12% (standard deviation [SD], +/- 1. 59%). In contrast, exposure to pollutants in the absence of P. multocida (groups B, D, and F) induced mild turbinate atrophy with mean MIs of 49.65% (SD, +/-1.96%), 51.04% (SD, +/-2.06%), and 49.88% (SD, +/-3.51%), respectively. A similar level of atrophy was also evoked by inoculation with P. multocida in the absence of pollutants (group G), giving a mean MI of 50.77% (SD, +/-2.07%). However, when P. multocida inoculation was combined with pollutant exposure (groups A, C, and E) moderate to severe turbinate atrophy occurred with mean MIs of 64.93% (SD, +/-4.64%), 59.18% (SD, +/-2.79%), and 73.30% (SD, +/-3.19%), respectively. The severity of atrophy was greatest in pigs exposed simultaneously to dust and ammonia. At the end of the exposure period, higher numbers of P. multocida bacteria were isolated from the tonsils than from the nasal membrane, per gram of tissue. The severity of turbinate atrophy in inoculated pigs was proportional to the number of P. multocida bacteria isolated from tonsils (r2 = 0.909, P < 0.05) and nasal membrane (r2 = 0.628, P < 0.05). These findings indicate that aerial pollutants contribute to the severity of lesions associated with atrophic rhinitis by facilitating colonization of the pig's upper respiratory tract by P. multocida and also by directly evoking mild atrophy. (+info)
Compliance and stability of the bronchial wall in a model of allergen-induced lung inflammation. (7/4583)Airway wall remodeling in response to inflammation might alter load on airway smooth muscle and/or change airway wall stability. We therefore determined airway wall compliance and closing pressures in an animal model. Weanling pigs were sensitized to ovalbumin (OVA; ip and sc, n = 6) and were subsequently challenged three times with OVA aerosol. Control pigs received 0.9% NaCl (n = 4) in place of OVA aerosol. Bronchoconstriction in vivo was assessed from lung resistance and dynamic compliance. Semistatic airway compliance was recorded ex vivo in isolated segments of bronchus, after the final OVA aerosol or 0.9% NaCl challenge. Internally or externally applied pressure needed to close bronchial segments was determined in the absence or presence of carbachol (1 microM). Sensitized pig lungs exhibited immediate bronchoconstriction to OVA aerosol and also peribronchial accumulations of monocytes and granulocytes. Compliance was reduced in sensitized bronchi in vitro (P < 0.01), and closing pressures were increased (P < 0.05). In the presence of carbachol, closing pressures of control and sensitized bronchi were not different. We conclude that sensitization and/or inflammation increases airway load and airway stability. (+info)
Qualitative and quantitative differences in T cell receptor binding of agonist and antagonist ligands. (8/4583)The kinetics of interaction between TCR and MHC-peptide show a general relationship between affinity and the biological response, but the reported kinetic differences between antigenic and antagonistic peptides are very small. Here, we show a remarkable difference in the kinetics of TCR interactions with strong agonist ligands at 37 degrees C compared to 25 degrees C. This difference is not seen with antagonist/positive selecting ligands. The interaction at 37 degrees C shows biphasic binding kinetics best described by a model of TCR dimerization. The altered kinetics greatly increase the stability of complexes with agonist ligands, accounting for the large differences in biological response compared to other ligands. Thus, there may be an allosteric, as well as a kinetic, component to the discrimination between agonists and antagonists. (+info)
The diagnosis of BHR is based on a combination of clinical, physiological, and imaging tests. The most common method used to assess BHR is the methacholine or histamine challenge test, which involves inhaling progressively increasing concentrations of these substances to measure airway reactivity. Other tests include exercise testing, hyperventilation, and mannitol challenge.
BHR is characterized by an increased responsiveness of the airways to various stimuli, such as allergens, cold or exercise, leading to inflammation and bronchoconstriction. This can cause symptoms such as wheezing, coughing, shortness of breath, and chest tightness.
There are several risk factors for BHR, including:
* Respiratory infections
* Exposure to environmental pollutants
* Genetic predisposition
Treatment of BHR typically involves the use of bronchodilators, corticosteroids, and other medications to reduce inflammation and airway constriction. In severe cases, surgical procedures such as lung volume reduction or bronchial thermoplasty may be necessary. Environmental modifications, such as avoiding triggers and using HEPA filters, can also help manage symptoms.
In summary, bronchial hyperreactivity is a condition characterized by an exaggerated response of the airways to various stimuli, leading to increased smooth muscle contraction and narrowing of the bronchi. It is commonly seen in asthma and other respiratory diseases, and can cause symptoms such as wheezing, coughing, shortness of breath, and chest tightness. Treatment typically involves medications and environmental modifications to reduce inflammation and airway constriction.
Respiratory hypersensitivity can be diagnosed through medical history, physical examination, and allergy testing. Treatment options include avoidance of allergens, medication, such as antihistamines or corticosteroids, and immunotherapy, which involves exposing the person to small amounts of the allergen over time to build up their tolerance.
Some people with respiratory hypersensitivity may experience more severe symptoms, such as asthma, which can be life-threatening if left untreated. It is important for individuals with respiratory hypersensitivity to work closely with their healthcare provider to manage their condition and prevent complications.
Asthma can cause recurring episodes of wheezing, coughing, chest tightness, and shortness of breath. These symptoms occur when the muscles surrounding the airways contract, causing the airways to narrow and swell. This can be triggered by exposure to environmental allergens or irritants such as pollen, dust mites, pet dander, or respiratory infections.
There is no cure for asthma, but it can be managed with medication and lifestyle changes. Treatment typically includes inhaled corticosteroids to reduce inflammation, bronchodilators to open up the airways, and rescue medications to relieve symptoms during an asthma attack.
Asthma is a common condition that affects people of all ages, but it is most commonly diagnosed in children. According to the American Lung Association, more than 25 million Americans have asthma, and it is the third leading cause of hospitalization for children under the age of 18.
While there is no cure for asthma, early diagnosis and proper treatment can help manage symptoms and improve quality of life for those affected by the condition.
There are several types of hypersensitivity reactions, including:
1. Type I hypersensitivity: This is also known as immediate hypersensitivity and occurs within minutes to hours after exposure to the allergen. It is characterized by the release of histamine and other chemical mediators from immune cells, leading to symptoms such as hives, itching, swelling, and difficulty breathing. Examples of Type I hypersensitivity reactions include allergies to pollen, dust mites, or certain foods.
2. Type II hypersensitivity: This is also known as cytotoxic hypersensitivity and occurs within days to weeks after exposure to the allergen. It is characterized by the immune system producing antibodies against specific proteins on the surface of cells, leading to their destruction. Examples of Type II hypersensitivity reactions include blood transfusion reactions and serum sickness.
3. Type III hypersensitivity: This is also known as immune complex hypersensitivity and occurs when antigens bind to immune complexes, leading to the formation of deposits in tissues. Examples of Type III hypersensitivity reactions include rheumatoid arthritis and systemic lupus erythematosus.
4. Type IV hypersensitivity: This is also known as delayed-type hypersensitivity and occurs within weeks to months after exposure to the allergen. It is characterized by the activation of T cells, leading to inflammation and tissue damage. Examples of Type IV hypersensitivity reactions include contact dermatitis and toxic epidermal necrolysis.
The diagnosis of hypersensitivity often involves a combination of medical history, physical examination, laboratory tests, and elimination diets or challenges. Treatment depends on the specific type of hypersensitivity reaction and may include avoidance of the allergen, medications such as antihistamines or corticosteroids, and immunomodulatory therapy.
There are several types of food hypersensitivity, including:
1. Food Allergy: An immune system reaction to a specific food that can cause symptoms ranging from mild hives to life-threatening anaphylaxis. Common food allergies include reactions to peanuts, tree nuts, fish, shellfish, milk, eggs, wheat, and soy.
2. Non-Allergic Food Hypersensitivity: Also known as non-IgE-mediated food hypersensitivity, this type of reaction does not involve the immune system. Symptoms can include bloating, abdominal pain, diarrhea, and headaches. Common culprits include gluten, dairy, and high-FODMAP foods.
3. Food Intolerance: A condition where the body cannot properly digest or process a specific food. Symptoms can include bloating, abdominal pain, diarrhea, and gas. Common food intolerances include lactose intolerance, fructose malabsorption, and celiac disease.
4. Food Aversion: An emotional response to a specific food that can cause avoidance or dislike of the food. This is not an allergic or physiological reaction but rather a psychological one.
The diagnosis of food hypersensitivity typically involves a thorough medical history, physical examination, and diagnostic tests such as skin prick testing or blood tests. Treatment options for food hypersensitivity depend on the type and severity of the reaction and may include avoidance of the offending food, medication, or immunotherapy.
Examples of delayed hypersensitivity reactions include contact dermatitis (a skin reaction to an allergic substance), tuberculin reactivity (a reaction to the bacteria that cause tuberculosis), and sarcoidosis (a condition characterized by inflammation in various organs, including the lungs and lymph nodes).
Delayed hypersensitivity reactions are important in the diagnosis and management of allergic disorders and other immune-related conditions. They can be detected through a variety of tests, including skin prick testing, patch testing, and blood tests. Treatment for delayed hypersensitivity reactions depends on the underlying cause and may involve medications such as antihistamines, corticosteroids, or immunosuppressants.
Symptoms of anaphylaxis include:
1. Swelling of the face, lips, tongue, and throat
2. Difficulty breathing or swallowing
3. Abdominal cramps
4. Nausea and vomiting
5. Rapid heartbeat
6. Feeling of impending doom or loss of consciousness
Anaphylaxis is diagnosed based on a combination of symptoms, medical history, and physical examination. Treatment for anaphylaxis typically involves administering epinephrine (adrenaline) via an auto-injector, such as an EpiPen or Auvi-Q. Additional treatments may include antihistamines, corticosteroids, and oxygen therapy.
Prevention of anaphylaxis involves avoiding known allergens and being prepared to treat a reaction if it occurs. If you have a history of anaphylaxis, it is important to carry an EpiPen or other emergency medication with you at all times. Wearing a medical alert bracelet or necklace can also help to notify others of your allergy and the need for emergency treatment.
In severe cases, anaphylaxis can lead to unconsciousness, seizures, and even death. Prompt treatment is essential to prevent these complications and ensure a full recovery.
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.
Airway remodeling is a complex process that involves changes in the structure and function of the airways, as well as an immune response. It is characterized by the following features:
* Airway wall thickening and inflammation
* Increased mucus production
* Narrowing of the airway lumina due to smooth muscle hypertrophy and fibrosis
* Increased airway resistance and decreased lung function.
Airway remodeling is a hallmark of asthma and COPD, and it can lead to exacerbations and poor disease control if left untreated. The exact mechanisms driving airway remodeling are not fully understood, but it is believed that a combination of genetic and environmental factors contribute to its development.
There are several techniques used to assess airway remodeling in patients with respiratory diseases, including:
* Quantitative computed tomography (QCT) - This technique allows for the measurement of airway wall thickness and luminal area.
* Magnetic resonance imaging (MRI) - MRI can provide information on airway size and shape, as well as tissue composition.
* Bronchoscopy with biopsy - This procedure allows for the examination of airway tissue and the assessment of inflammation and fibrosis.
There are several treatments available for airway remodeling in patients with respiratory diseases, including:
* Medications such as bronchodilators, corticosteroids, and anti-inflammatory drugs
* Pulmonary rehabilitation - This includes exercises and education to help improve lung function and overall health.
* Lung transplantation - In severe cases of airway remodeling that do not respond to other treatments, lung transplantation may be considered.
It is important for patients with respiratory diseases to work closely with their healthcare provider to monitor their condition and adjust their treatment plan as needed. With appropriate management, many patients with airway remodeling can experience improved lung function and quality of life.
The diagnosis of pulmonary eosinophilia is based on a combination of clinical symptoms, physical examination findings, and laboratory tests such as chest X-rays, blood tests, and bronchoalveolar lavage (BAL) fluid analysis.
Treatment of pulmonary eosinophilia depends on the underlying cause and may include medications such as corticosteroids, antihistamines, or antibiotics, as well as lifestyle modifications such as avoiding allergens and managing stress. In severe cases, hospitalization may be necessary to monitor and treat the condition.
Some common symptoms of pulmonary eosinophilia include:
* Shortness of breath (dyspnea)
* Chest tightness or discomfort
* Recurrent respiratory infections
Complications of pulmonary eosinophilia can include:
* Respiratory failure
* Asthma exacerbation
* Chronic obstructive pulmonary disease (COPD)
* Pneumonia or other respiratory infections
* Airway obstruction
It is important to seek medical attention if you experience any of these symptoms, as early diagnosis and treatment can help prevent complications and improve outcomes.
There are many possible causes of eosinophilia, including:
* Parasitic infections
* Autoimmune disorders
The symptoms of eosinophilia can vary depending on the underlying cause, but may include:
* Swelling of the skin, lips, and eyes
* Hives or itchy skin
* Shortness of breath or wheezing
* Abdominal pain
Eosinophilia is typically diagnosed through a blood test that measures the number of eosinophils in the blood. Other tests such as imaging studies, skin scrapings, and biopsies may also be used to confirm the diagnosis and identify the underlying cause.
The treatment of eosinophilia depends on the underlying cause, but may include medications such as antihistamines, corticosteroids, and chemotherapy. In some cases, removal of the causative agent or immunomodulatory therapy may be necessary.
Eosinophilia can lead to a number of complications, including:
* Anaphylaxis (a severe allergic reaction)
* Eosinophilic granulomas (collections of eosinophils that can cause organ damage)
* Eosinophilic gastrointestinal disorders (conditions where eosinophils invade the digestive tract)
The prognosis for eosinophilia depends on the underlying cause, but in general, the condition is not life-threatening. However, if left untreated, complications can arise and the condition can have a significant impact on quality of life.
In conclusion, eosinophilia is a condition characterized by an abnormal increase in eosinophils in the body. While it can be caused by a variety of factors, including allergies, infections, and autoimmune disorders, the underlying cause must be identified and treated in order to effectively manage the condition and prevent complications.
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.
Synonyms: Bronchial Constriction, Airway Spasm, Reversible Airway Obstruction.
Antonyms: Bronchodilation, Relaxation of Bronchial Muscles.
1. The patient experienced bronchial spasms during the asthma attack and was treated with an inhaler.
2. The bronchial spasm caused by the allergic reaction was relieved by administering epinephrine.
3. The doctor prescribed corticosteroids to reduce inflammation and prevent future bronchial spasms.
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:
3. Heart disease
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.
Egg hypersensitivity can be caused by either an immunoglobulin E (IgE) or non-IgE mechanism. IgE is an antibody produced by the immune system in response to an allergen, and it is responsible for triggering the allergic reaction. Non-IgE mechanisms are not well understood but may involve other immune cells such as T cells and macrophages.
The symptoms of egg hypersensitivity can vary from person to person and may range from mild to severe. In addition to anaphylaxis, they may include:
* Hives or itchy skin
* Swelling of the face, lips, tongue, or throat
* Difficulty breathing or swallowing
* Abdominal cramps
Egg hypersensitivity can be diagnosed through a variety of tests, including:
* Skin prick test (SPT): This is the most common method of testing for egg hypersensitivity. It involves placing a small amount of egg protein on the skin and then pricking the skin with a small needle to allow the protein to enter the body. If a person is allergic to eggs, a raised bump or hive will appear within 15-20 minutes.
* Blood test: A blood test can measure the levels of immunoglobulin E (IgE) antibodies in the blood, which are responsible for triggering the allergic reaction. High levels of IgE antibodies indicate an egg hypersensitivity.
* Food challenge: This involves feeding a person increasing amounts of egg to see if they experience any symptoms.
There is no cure for egg hypersensitivity, but there are several treatments available to manage the symptoms. These include:
* Avoidance: The best way to manage egg hypersensitivity is to avoid eggs altogether. This can be challenging, as eggs are a common ingredient in many foods.
* Antihistamines: These medications can help relieve mild to moderate symptoms such as hives and itching.
* Corticosteroids: These medications can help reduce inflammation and swelling.
* Epinephrine injectors: These devices administer a dose of epinephrine, which can help reverse severe symptoms such as anaphylaxis.
* Immunotherapy: This involves exposing the person to small amounts of egg protein over time to build up their tolerance to the allergen.
It is important to note that egg hypersensitivity can be life-threatening, especially in cases of anaphylaxis. Therefore, it is crucial to seek medical attention immediately if symptoms persist or worsen over time.
Chicken ovalbumin upstream promoter-transcription factor
Margaret Oakley Dayhoff
Plasminogen activator inhibitor-2
Inhibition of an established allergic response to ovalbumin in BALB/c mice by killed Mycobacterium vaccae
Poly [D, L-lactide-co-glycolide] Microspheres as a Delivery System of Protein Ovalbumin Used as a Model Protein Drug
OVALBUMIN | Bioseutica®
egg ovalbumin OVA (323-339) peptide control peptide | Technique alternative | 01011972186 - Conzort
Synthesis of an ovalbumin-like protein by Escherichia coli K12 harbouring a recombinant plasmid - Wikidata
Gekko gecko extract attenuates airway inflammation and mucus hypersecretion in a murine model of ovalbumin-induced asthma. | J...
Hypersensitivity of vagal pulmonary C-fibers induced by increasing airway temperature in ovalbumin-sensitized rats<...
Prevention and Control of Influenza with Vaccines: Recommendations of the Advisory Committee on Immunization Practices, United...
Bee venom phospholipase A2 suppresses allergic airway inflammation in an ovalbumin-induced asthma model through the induction...
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Epoxyeicosatrienoic acids are involved in the C70 fullerene derivative-induced control of allergic asthma, NC DOCKS (North...
Measles and Mumps Vaccines - Adverse Events Associated with Childhood Vaccines - NCBI Bookshelf
The receptor NLRP3 is a transcriptional regulator of TH2 differentiation | Nature Immunology
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NIOSHTIC-2 Search Results - Full View
Bacterial Protein in House Dust May Spur Asthma | National Institutes of Health (NIH)
InvivoGen: Reagents and Tools for Cell Biology Research
Genre: Slides (photographs) - Harold Varmus - Profiles in Science Search Results
Vaccine Safety References | Children's Hospital of Philadelphia
SciELO - Brazil - Bromelain: Methods of Extraction, Purification and Therapeutic Applications Bromelain: Methods of Extraction...
Lipid-Polymer Hybrid Nanoparticles Utilize B Cells and Dendritic Cells to Elicit Distinct Antigen-Specific CD4+ and CD8+ T Cell...
Pulmonary anti-inflammatory effects and spasmolytic properties of Costa Rican noni juice (Morinda citrifolia L.) - PubMed
Inactivated Whole Virus Influenza A (H5N1) Vaccine - Volume 13, Number 5-May 2007 - Emerging Infectious Diseases journal - CDC
Researchers suggest link between BPA exposure and food intolerance
- In this study, the effect of aerosolised honey on airway tissues in a rabbit model of ovalbumin (OVA)-induced asthma was investigated. (nih.gov)
- Background: We have previously shown that lipopolysaccharide (LPS) exposure in sensitised animals 18 h after ovalbumin (OVA) challenge inhibits OVA-induced airway hyper-responsiveness (AHR). (edu.au)
- Attenuates Oxidative Stress and Airway Inflammation in a Murine Model of Ovalbumin-Challenged Asthma. (bvsalud.org)
- Lindera obtusiloba Attenuates Oxidative Stress and Airway Inflammation in a Murine Model of Ovalbumin-Challenged Asthma. (bvsalud.org)
- Bee venom phospholipase A2 suppresses allergic airway inflammation in an ovalbumin-induced asthma model through the induction of regulatory T cells. (bioseek.eu)
- Mice inhaling either ovalbumin alone or any of a series of microbial products alone didn't have airway reactions. (nih.gov)
- However, when given together, certain products caused some mice to become sensitized to ovalbumin and develop airway inflammation when later exposed. (nih.gov)
- The scientists saw particularly strong allergic airway responses in mice receiving ovalbumin together with a bacterial protein called flagellin. (nih.gov)
- Here, we investigated whether endogenous apo A-I modulates ovalbumin (OVA)-induced neutrophilic airway inflammation in mice. (nih.gov)
- We conclude that endogenous apoA-I negatively regulates key pathways that mediate the chemotaxis, vascular adhesion and survival of neutrophils in ovalbumin-induced airway inflammation. (nih.gov)
- Cysteine (CYSH), glutathione (GSH), and markers of inflammation in bronchoalveolar lavage fluid (BALF) were measured following ovalbumin (OVA) inhalation challenge. (cdc.gov)
- Here, ovalbumin was used as a model protein drug. (scialert.net)
- In vitro protein release study showed that release profile of ovalbumin from biodegradable microspheres varied due to the change in homogenizing speeds during multiple emulsion preparation technique. (scialert.net)
- PLGA microspheres containing ovalbumin as a model protein could be useful for the controlled delivery of similar protein drugs. (scialert.net)
- The purpose of the present study was to develop protein (ovalbumin)-loaded microspheres with biodegradable polymer, poly (D,L-lactide-co-glycolide) (PLGA) and standardization of various process parameters such as homogenizing speed during preparations, particle surface morphology and surface charges, particle size and in vitro protein release to obtain microspheres with maximum protein-loading and minimum polydispersion with a maximally sustained protein release pattern. (scialert.net)
- OVALBUMIN is the predominant egg-white protein, comprising 54% of the total. (bioseutica.com)
- Ovalbumin (abbreviated OVA) is the main protein found in egg white, making up 60-65% of the total protein. (conzort.com)
- The function of ovalbumin is unknown, although it is presumed to be a storage protein. (conzort.com)
- The scientists used an innocuous protein called ovalbumin for their screen. (nih.gov)
- Objective: In the present study, the anti-allergic effect of OR extract was evaluated on an ovalbumin (OVA)-induced allergic rhinitis in mice and rat peritoneal mast cells (RPMC). (who.int)
- The study was conducted to investigate the promoted immune response to ovalbumin in mice by chitosan nanoparticles (CNP) and its toxicity. (mdpi.com)
- Institute of Cancer Research (ICR) mice were immunized subcutaneously with 25 μg ovalbumin (OVA) alone or with 25 μg OVA dissolved in saline containing Quil A (10 μg), chitosan (CS) (50 μg) or CNP (12.5, 50 or 200 μg) on days 1 and 15. (mdpi.com)
- Here, we report that AhR-deficient mice develop increased allergic responses to the model allergen ovalbumin (OVA), which are driven in part by increased dendritic cell (DC) functional activation. (nih.gov)
- on ovalbumin-induced asthma mice. (nih.gov)
- In this study we evaluated the effect of 1'-acetoxychavicol acetate (ACA) isolated from Alpinia galanga rhizomes in a mouse model of ovalbumin (OVA)-induced asthma. (nih.gov)
- In this study, we investigated anti-inflammatory and anti-oxidant effects of the methanolic extract of L. obtusiloba leaves (LOL) in an ovalbumin ( OVA )-challenged allergic asthma model and tumor necrosis factor (TNF)-α-stimulated NCI-H292 cell . (bvsalud.org)
- The full-length pigeon ovalbumin (OVA) gene cDNA was cloned and sequenced by reverse transcription-polymerase chain reaction (RT-PCR) and rapid-amplification of cDNA ends. (geneticsmr.com)
- Antiallergic effect of Ostericum koreanum root extract on ovalbumin-induced allergic rhinitis mouse model and mast cells. (who.int)
- This study was carried out to test the hypothesis that HWA enhances the pulmonary C-fiber sensitivity in Brown-Norway rats sensitized with ovalbumin (Ova). (uky.edu)
- The Chicken egg ovalbumin OVA (323-339) peptide control peptide is manufactured for Research Use Only or for diagnostics purposes. (conzort.com)
- The pulmonary effects of two environmentally relevant aldehydes were investigated in ovalbumin (OA)-sensitized guinea-pigs (GP). (archives-ouvertes.fr)
- ovalbumin content is ≤3 ng/dose (1 mL), based on ELISA. (nih.gov)
- To revise the Ovalbumin test release specification and make the associated changes to the labeling. (cdc.gov)