Tumor Necrosis Factor-alpha
Liver Diseases, Alcoholic
Rats, Inbred Strains
Drug-Induced Liver Injury
Mononuclear Phagocyte System
Liver Cirrhosis, Experimental
Pronase destroys the lipopolysaccharide receptor CD14 on Kupffer cells. (1/1142)CD14 is a lipopolysaccharide (LPS) receptor distributed largely in macrophages, monocytes, and neutrophils; however, the role of CD14 in activation of Kupffer cells by LPS remains controversial. The purpose of this study was to determine if different methods used to isolate Kupffer cells affect CD14. Kupffer cells were isolated by collagenase (0.025%) or collagenase-Pronase (0.02%) perfusion and differential centrifugation using Percoll gradients and cultured for 24 h before experiments. CD14 mRNA was detected by RT-PCR from Kupffer cell total RNA as well as from peritoneal macrophages. Western blotting showed that Kupffer cells prepared with collagenase possess CD14; however, it was absent in cells obtained by collagenase-Pronase perfusion. Intracellular calcium in Kupffer cells prepared with collagenase was increased transiently to levels around 300 nM by addition of LPS with 5% rat serum, which contains LPS binding protein. This increase in intracellular calcium was totally serum dependent. Moreover, LPS-induced increases in intracellular calcium in Kupffer cells were blunted significantly (40% of controls) when cells were treated with phosphatidylinositol-specific phospholipase C, which cleaves CD14 from the plasma membrane. However, intracellular calcium did not increase when LPS was added to cells prepared by collagenase-Pronase perfusion even in the presence of serum. These cells were viable, however, because ATP increased intracellular calcium to the same levels as cells prepared with collagenase perfusion. Tumor necrosis factor-alpha (TNF-alpha) mRNA was increased in Kupffer cells prepared with collagenase perfusion 1 h after addition of LPS, an effect potentiated over twofold by serum; however, serum did not increase TNF-alpha mRNA in cells isolated via collagenase-Pronase perfusion. Moreover, treatment with Pronase rapidly decreased CD14 on mouse macrophages (RAW 264.7 cells) and Kupffer cells. These findings indicate that Pronase cleaves CD14 from Kupffer cells, whereas collagenase perfusion does not, providing an explanation for why Kupffer cells do not exhibit a CD14-mediated pathway when prepared with procedures using Pronase. It is concluded that Kupffer cells indeed contain a functional CD14 LPS receptor when prepared gently. (+info)
Effects of Ro 31-8220 on lipopolysaccharides-induced hepatotoxicity and release of tumor necrosis factor from rat Kupffer cells. (2/1142)AIM: To investigate protein kinase C (PKC) functions on lipopolysaccharide (LPS)-induced hepatotoxicity, a new potent PKC inhibitor Ro 31-8220 (Ro) was used to detect its effect on LPS-induced hepatotoxicity in rat hepatocytes and tumor necrosis factor (TNF) release from rat Kupffer cells (KC). METHODS: Hepatocytes (containing KC) were incubated with LPS (10 mg.L-1) and Ro (0.1-10 mumol.L-1) for 24 h, alanine aminotransferase (AlaA) leakage in the culture as indication of hepatotoxicity. The TNF activity in the supernatant of rat KC culture with LPS in the presence of Ro (0.1-10 mumol.L-1) was monitored by the L929 target cell lytic assay. RESULTS: Ro (0.1-10 mumol.L-1) reduced AlaA leakage in the hepatocyte culture. Ro inhibited dose-dependently the LPS-induced TNF production from rat KC. CONCLUSION: PKC inhibitor Ro protects the hepatocytes from LPS-induced cytotoxicity and inhibits the LPS-induced TNF production from rat KC. (+info)
Influences of Kupffer cell stimulation and suppression on immunological liver injury in mice. (3/1142)AIM: To study the possible involvement of Kupffer cells (KC) in immunological liver injury in mice. METHODS: Liver injury was induced by i.v. injection of Bacillus Calmette-Guerin (BCG) 5 x 10(7) viable bacilli followed by i.v. injection of lipopolysaccharides (LPS) 7.5 micrograms to each mouse. Indian ink and silica were i.v. injected to suppress KC and retinol was given po to stimulate KC in these mice. Plasma alanine aminotransferase (AlaAT), aspatate aminotransferase (AspAT), nitric oxide (NO), and liver tissue were examined. RESULTS: Injection of LPS following BCG injection resulted in a remarkable elevation of plasma NO, AlaAT, and AspAT levels, and severe liver damage. The damages were enhanced by the activation of KC with retinol and reduced by suppression of KC with silica and Indian ink. CONCLUSION: The degree of liver injury induced by BCG + LPS is closely correlated with the status of KC, and NO from KC plays an important role in the pathogenesis of the liver damage in mice. (+info)
Febrile-range temperature modifies early systemic tumor necrosis factor alpha expression in mice challenged with bacterial endotoxin. (4/1142)Fever improves survival in acute infections, but the effects of increased core temperature on host defenses are poorly understood. Tumor necrosis factor alpha (TNF-alpha) is an early activator of host defenses and a major endogenous pyrogen. TNF-alpha expression is essential for survival in bacterial infections but, if disregulated, can cause tissue injury. In this study, we show that passively increasing core temperature in mice from the basal (36.5 to 37.5 degrees C) to the febrile (39.5 to 40 degrees C) range modifies systemic TNF-alpha expression in response to bacterial endotoxin (lipopolysaccharide). The early TNF-alpha secretion rate is enhanced, but the duration of maximal TNF-alpha production is shortened. We identified Kupffer cells as the predominant source of the excess TNF-alpha production in the warmer animals. The enhanced early TNF-alpha production observed at the higher temperature in vivo could not be demonstrated in isolated Kupffer cells or in precision-cut liver slices in vitro, indicating the participation of indirect pathways. Therefore, expression of the endogenous pyrogen TNF-alpha is regulated by increments in core temperature during fever, generating an enhanced early, self-limited TNF-alpha pulse. (+info)
Intravenous glycine improves survival in rat liver transplantation. (5/1142)In situ manipulation by touching, retracting, and moving liver lobes gently during harvest dramatically reduces survival after transplantation (P. Schemmer, R. Schoonhoven, J. A. Swenberg, H. Bunzendahl, and R. G. Thurman. Transplantation 65: 1015-1020, 1998). The development of harvest-dependent graft injury upon reperfusion can be prevented with GdCl3, a rare earth metal and Kupffer cell toxicant, but it cannot be used in clinical liver transplantation because of its potential toxicity. Thus the effect of glycine, which prevents activation of Kupffer cells, was assessed here. Minimal dissection of the liver for 12 min plus 13 min without manipulation had no effect on survival (100%). However, gentle manipulation decreased survival to 46% in the control group. Furthermore, serum transaminases and liver necrosis were elevated 4- to 12-fold 8 h after transplantation. After organ harvest, the rate of entry and exit of fluorescein dextran, a dye confined to the vascular space, was decreased about twofold, indicating disturbances in the hepatic microcirculation. Pimonidazole binding, which detects hypoxia, increased about twofold after organ manipulation, and Kupffer cells isolated from manipulated livers produced threefold more tumor necrosis factor-alpha after lipopolysaccharide than controls. Glycine given intravenously to the donor increased the serum glycine concentration about sevenfold and largely prevented the effect of gentle organ manipulation on all parameters studied. These data indicate for the first time that pretreatment of donors with intravenous glycine minimizes reperfusion injury due to organ manipulation during harvest and after liver transplantation. (+info)
A comparison of the pharmacological properties of carbohydrate remodeled recombinant and placental-derived beta-glucocerebrosidase: implications for clinical efficacy in treatment of Gaucher disease. (6/1142)The objective of these studies was to characterize the macrophage mannose receptor binding and pharmacological properties of carbohydrate remodeled human placental-derived and recombinant beta-glucocerebrosidase (pGCR and rGCR, respectively). These are similar but not identical molecules that were developed as enzyme replacement therapies for Gaucher disease. Both undergo oligosaccharide remodeling during purification to expose terminal mannose sugar residues. Competitive binding data indicated carbohydrate remodeling improved targeting to mannose receptors over native enzyme by two orders of magnitude. Mannose receptor dissociation constants (Kd) for pGCR and rGCR were each 13 nmol/L. At 37 degrees C, 95% of the total macrophage binding was mannose receptor specific. In vivo, pGCR and rGCR were cleared from circulation by a saturable pathway. The serum half-life (t1/2) was 3 minutes when less than saturable amounts were injected intravenously (IV) into mice. Twenty minutes postdose, beta-glucocerebrosidase activity increased over endogenous levels in all tissues examined. Fifty percent of the injected activity was recovered. Ninety-five percent of recovered activity was in the liver. Parenchymal cells (PC), Kupffer cells (KC), and liver endothelium cells (LEC) were responsible for 75%, 22%, and 3%, respectively, of the hepatocellular uptake of rGCR and for 76%, 11%, and 12%, respectively, of the hepatocellular uptake of pGCR. Both molecules had poor stability in LEC and relatively long terminal half-lives in PC (t1/2 = 2 days) and KC (t1/2 = 3 days). (+info)
Infection of primary cultures of human Kupffer cells by Dengue virus: no viral progeny synthesis, but cytokine production is evident. (7/1142)We investigated the ability of dengue virus to invade human primary Kupffer cells and to complete its life cycle. The virus effectively penetrated Kupffer cells, but the infection did not result in any viral progeny. Dengue virus-replicating Kupffer cells underwent apoptosis and were cleared by phagocytosis. Infected Kupffer cells produced soluble mediators that could intervene in dengue virus pathogenesis. (+info)
Prevention of Kupffer cell-induced oxidant injury in rat liver by atrial natriuretic peptide. (8/1142)The generation of reactive oxygen species (ROS) by activated Kupffer cells contributes to liver injury following liver preservation, shock, or endotoxemia. Pharmacological interventions to protect liver cells against this inflammatory response of Kupffer cells have not yet been established. Atrial natriuretic peptide (ANP) protects the liver against ischemia-reperfusion injury, suggesting a possible modulation of Kupffer cell-mediated cytotoxicity. Therefore, we investigated the mechanism of cytoprotection by ANP during Kupffer cell activation in perfused rat livers of male Sprague-Dawley rats. Activation of Kupffer cells by zymosan (150 microgram/ml) resulted in considerable cell damage, as assessed by the sinusoidal release of lactate dehydrogenase and purine nucleoside phosphorylase. Cell damage was almost completely prevented by superoxide dismutase (50 U/ml) and catalase (150 U/ml), indicating ROS-related liver injury. ANP (200 nM) reduced Kupffer cell-induced injury via the guanylyl cyclase-coupled A receptor (GCA receptor) and cGMP: mRNA expression of the GCA receptor was found in hepatocytes, endothelial cells, and Kupffer cells, and the cGMP analog 8-bromo-cGMP (8-BrcGMP; 50 microM) was as potent as ANP in protecting from zymosan-induced cell damage. ANP and 8-BrcGMP significantly attenuated the prolonged increase of hepatic vascular resistance when Kupffer cell activation occurred. Furthermore, both compounds reduced oxidative cell damage following infusion of H2O2 (500 microM). In contrast, superoxide anion formation of isolated Kupffer cells was not affected by ANP and only moderately reduced by 8-BrcGMP. In conclusion, ANP protects the liver against Kupffer cell-related oxidant stress. This hormonal protection is mediated via the GCA receptor and cGMP, suggesting that the cGMP receptor plays a critical role in controlling oxidative cell damage. Thus ANP signaling should be considered as a new pharmacological target for protecting liver cells against the inflammatory response of activated Kupffer cells without eliminating the vital host defense function of these cells. (+info)
Gadolinium is a chemical element that is commonly used in the medical field as a contrast agent for magnetic resonance imaging (MRI) scans. It is a paramagnetic metal that enhances the visibility of certain structures in the body on MRI images. When gadolinium is administered to a patient, it binds to proteins in the body and becomes concentrated in areas with high blood flow, such as blood vessels and tumors. This increased concentration of gadolinium in these areas makes them more visible on MRI images, allowing doctors to better diagnose and monitor a variety of medical conditions, including cancer, cardiovascular disease, and neurological disorders. Gadolinium-based contrast agents are generally considered safe and effective when used as directed. However, in some cases, patients may experience adverse reactions to gadolinium, such as allergic reactions or nephrogenic systemic fibrosis (NSF), a rare but serious condition that can cause skin thickening and scarring. As a result, healthcare providers must carefully weigh the benefits and risks of gadolinium use on a case-by-case basis.
Clodronic acid is a bisphosphonate medication that is used to treat and prevent osteoporosis, a condition in which the bones become weak and brittle. It works by inhibiting the activity of osteoclasts, which are cells that break down bone tissue. This helps to slow down bone loss and increase bone density. Clodronic acid is also used to treat Paget's disease of the bone, a condition in which the bone tissue is overactive and causes the bones to become enlarged and misshapen. It is usually taken orally in the form of tablets or as a solution that is injected into a vein.
Lipopolysaccharides (LPS) are a type of complex carbohydrate found on the surface of gram-negative bacteria. They are composed of a lipid A moiety, a core polysaccharide, and an O-specific polysaccharide. LPS are important components of the bacterial cell wall and play a role in the innate immune response of the host. In the medical field, LPS are often studied in the context of sepsis, a life-threatening condition that occurs when the body's response to an infection causes widespread inflammation. LPS can trigger a strong immune response in the host, leading to the release of pro-inflammatory cytokines and other mediators that can cause tissue damage and organ failure. As a result, LPS are often used as a model for studying the pathophysiology of sepsis and for developing new treatments for this condition. LPS are also used in research as a tool for studying the immune system and for developing vaccines against bacterial infections. They can be purified from bacterial cultures and used to stimulate immune cells in vitro or in animal models, allowing researchers to study the mechanisms of immune responses to bacterial pathogens. Additionally, LPS can be used as an adjuvant in vaccines to enhance the immune response to the vaccine antigen.
Tumor Necrosis Factor-alpha (TNF-alpha) is a cytokine, a type of signaling protein, that plays a crucial role in the immune response and inflammation. It is produced by various cells in the body, including macrophages, monocytes, and T cells, in response to infection, injury, or other stimuli. TNF-alpha has multiple functions in the body, including regulating the immune response, promoting cell growth and differentiation, and mediating inflammation. It can also induce programmed cell death, or apoptosis, in some cells, which can be beneficial in fighting cancer. However, excessive or prolonged TNF-alpha production can lead to chronic inflammation and tissue damage, which can contribute to the development of various diseases, including autoimmune disorders, inflammatory bowel disease, and certain types of cancer. In the medical field, TNF-alpha is often targeted in the treatment of these conditions. For example, drugs called TNF inhibitors, such as infliximab and adalimumab, are used to block the action of TNF-alpha and reduce inflammation in patients with rheumatoid arthritis, Crohn's disease, and other inflammatory conditions.
In the medical field, "Poly I" typically refers to a type of nucleic acid called polyinosinic acid, which is a synthetic polymer of the nucleotide adenosine monophosphate (AMP) with the base inosine (I). Polyinosinic acid is often used in research and clinical applications as a control or reference material for nucleic acid analysis, such as in the detection and quantification of viral or bacterial infections. It is also used as a component of gene therapy vectors, where it can help protect the therapeutic gene from degradation and enhance its expression in target cells. Overall, "Poly I" is a useful tool in the field of molecular biology and medicine, and its applications continue to expand as new technologies and techniques are developed.
Hepatitis is a medical condition characterized by inflammation of the liver. It can be caused by a variety of factors, including viral infections, alcohol abuse, drug toxicity, autoimmune disorders, and inherited metabolic disorders. There are several types of hepatitis, including: 1. Hepatitis A: caused by the hepatitis A virus (HAV) and typically spreads through contaminated food or water. 2. Hepatitis B: caused by the hepatitis B virus (HBV) and can be transmitted through sexual contact, sharing needles, or from mother to child during childbirth. 3. Hepatitis C: caused by the hepatitis C virus (HCV) and is primarily transmitted through sharing needles or other equipment used for injecting drugs. 4. Hepatitis D: caused by the hepatitis D virus (HDV) and can only occur in people who are already infected with HBV. 5. Hepatitis E: caused by the hepatitis E virus (HEV) and is typically transmitted through contaminated food or water. Symptoms of hepatitis can include fatigue, nausea, vomiting, abdominal pain, dark urine, and yellowing of the skin and eyes (jaundice). In some cases, hepatitis can be asymptomatic or cause only mild symptoms. Treatment for hepatitis depends on the underlying cause and can include antiviral medications, lifestyle changes, and in severe cases, liver transplantation. It is important to seek medical attention if you suspect you may have hepatitis, as early diagnosis and treatment can help prevent complications and improve outcomes.
Alcoholic liver disease (ALD) is a group of conditions that affect the liver as a result of excessive alcohol consumption. It is a common and serious health problem worldwide, and can lead to a range of complications, including cirrhosis, liver failure, and liver cancer. ALD can be classified into three main categories: fatty liver, alcoholic hepatitis, and cirrhosis. Fatty liver is the earliest stage of ALD, characterized by the accumulation of fat in liver cells. Alcoholic hepatitis is a more severe form of ALD, characterized by inflammation and damage to liver cells. Cirrhosis is the final stage of ALD, characterized by the replacement of healthy liver tissue with scar tissue, which can lead to liver failure. The symptoms of ALD can vary depending on the stage of the disease, but may include fatigue, weakness, abdominal pain, jaundice, and loss of appetite. Treatment for ALD typically involves stopping alcohol consumption, as well as supportive care to manage symptoms and prevent complications. In some cases, medications or liver transplantation may be necessary.
Drug-induced liver injury (DILI) is a type of liver damage that occurs as a result of taking medications or other substances. It can range from mild to severe and can be caused by a variety of drugs, including antibiotics, painkillers, and certain herbal supplements. DILI can present with a range of symptoms, including nausea, vomiting, abdominal pain, jaundice (yellowing of the skin and eyes), and dark urine. In severe cases, DILI can lead to liver failure, which can be life-threatening. Diagnosis of DILI typically involves a combination of clinical examination, laboratory tests, and imaging studies. Treatment may involve discontinuing the suspected drug, administering supportive care, and in severe cases, liver transplantation. Preventing DILI involves careful monitoring of patients who are taking medications that have the potential to cause liver damage, as well as educating patients about the potential risks and symptoms of DILI.
Liver diseases refer to a wide range of medical conditions that affect the liver, which is a vital organ responsible for many essential functions in the body. These diseases can be caused by various factors, including viral infections, alcohol abuse, drug toxicity, autoimmune disorders, genetic mutations, and metabolic disorders. Some common liver diseases include: 1. Hepatitis: An inflammation of the liver caused by a viral infection, such as hepatitis A, B, or C. 2. Cirrhosis: A chronic liver disease characterized by the scarring and hardening of liver tissue, which can lead to liver failure. 3. Non-alcoholic fatty liver disease (NAFLD): A condition in which excess fat accumulates in the liver, often as a result of obesity, insulin resistance, or a high-fat diet. 4. Alcoholic liver disease (ALD): A group of liver diseases caused by excessive alcohol consumption, including fatty liver, alcoholic hepatitis, and cirrhosis. 5. Primary biliary cholangitis (PBC): A chronic autoimmune liver disease that affects the bile ducts in the liver. 6. Primary sclerosing cholangitis (PSC): A chronic autoimmune liver disease that affects the bile ducts in the liver and can lead to cirrhosis. 7. Wilson's disease: A genetic disorder that causes copper to accumulate in the liver and other organs, leading to liver damage and other health problems. 8. Hemochromatosis: A genetic disorder that causes the body to absorb too much iron, leading to iron overload in the liver and other organs. Treatment for liver diseases depends on the underlying cause and severity of the condition. In some cases, lifestyle changes such as diet and exercise may be sufficient to manage the disease. In more severe cases, medications, surgery, or liver transplantation may be necessary.
Zymosan is a polysaccharide derived from the cell walls of yeasts and other fungi. It is commonly used in medical research as an activator of the immune system, particularly in the study of inflammation and autoimmune diseases. When zymosan is injected into the body, it triggers an immune response that involves the release of various inflammatory mediators, such as cytokines and chemokines. This response can be used to study the function of immune cells and the signaling pathways involved in inflammation. Zymosan has also been used in clinical trials as a potential treatment for various conditions, including rheumatoid arthritis, psoriasis, and sepsis. However, more research is needed to fully understand its therapeutic potential and potential side effects.
CD14 is a protein that is expressed on the surface of certain cells in the immune system, including macrophages and monocytes. It is a receptor for lipopolysaccharide (LPS), a component of the cell wall of certain types of bacteria. When CD14 binds to LPS, it triggers a signaling cascade that activates the immune system and leads to the production of pro-inflammatory cytokines. CD14 is also involved in the recognition and processing of other types of antigens, including bacterial and viral proteins. In the medical field, CD14 is often used as a marker for the activation of the innate immune system and is studied in the context of various diseases, including sepsis, infectious diseases, and cancer.
In the medical field, "latex" refers to a type of rubber that is commonly used to make medical equipment and supplies, such as gloves, catheters, and surgical instruments. Latex is a natural polymer that is derived from the sap of the rubber tree, and it is known for its strength, elasticity, and resistance to chemicals and heat. However, some people may be allergic to latex, which can cause a range of symptoms from mild itching to severe allergic reactions such as anaphylaxis. As a result, many medical facilities have started to use alternative materials, such as nitrile or vinyl, for medical equipment and supplies to accommodate individuals with latex allergies.
Alanine transaminase (ALT) is an enzyme that plays a crucial role in the metabolism of amino acids in the liver. It is also known as alanine aminotransferase (ALT) and is found in high concentrations in liver cells. When liver cells are damaged or destroyed, ALT is released into the bloodstream, where it can be measured in a blood test. Elevated levels of ALT in the blood are often an indication of liver damage or disease, such as hepatitis, cirrhosis, or fatty liver disease. ALT is also found in other tissues, including the heart, skeletal muscle, and kidneys, but in lower concentrations than in the liver. In these tissues, elevated levels of ALT can indicate injury or disease. Overall, ALT is an important biomarker for liver function and can be used to diagnose and monitor liver diseases.
Receptors, Scavenger are proteins that are present on the surface of cells and are responsible for recognizing and binding to specific molecules, such as waste products or toxins, in the body. These receptors then internalize the bound molecules and transport them to the cell's interior for degradation or elimination. Scavenger receptors play an important role in maintaining the health of cells and tissues by removing harmful substances from the body. They are found in a variety of cell types, including macrophages, neutrophils, and endothelial cells.
Liver Cirrhosis, Experimental refers to a condition in which the liver becomes scarred and damaged due to various experimental procedures or treatments. This can occur in laboratory animals or humans who are undergoing medical research or clinical trials. Experimental liver cirrhosis can be induced by various methods, such as administering toxins, viruses, or other substances that cause liver damage. The purpose of such experiments is to study the pathophysiology of liver disease and to develop new treatments or therapies. The severity and extent of liver damage in experimental liver cirrhosis can vary depending on the type and duration of the experimental procedure. In some cases, the liver damage may be reversible, while in others, it may be irreversible and lead to liver failure or death. It is important to note that experimental liver cirrhosis is a controlled and regulated process that is conducted under strict ethical guidelines to minimize harm to the animals or humans involved.
Reperfusion injury is a type of damage that occurs when blood flow is restored to an organ or tissue that has been deprived of oxygen for a prolonged period of time. This can happen during a heart attack, stroke, or other conditions that cause blood flow to be blocked to a particular area of the body. When blood flow is restored, it can cause an inflammatory response in the affected tissue, leading to the release of free radicals and other harmful substances that can damage cells and tissues. This can result in a range of symptoms, including swelling, pain, and organ dysfunction. Reperfusion injury can be particularly damaging to the heart and brain, as these organs are highly sensitive to oxygen deprivation and have a limited ability to repair themselves. Treatment for reperfusion injury may involve medications to reduce inflammation and prevent further damage, as well as supportive care to manage symptoms and promote healing.
Receptors, Lipoprotein are proteins that are present on the surface of cells and are responsible for binding to lipoproteins, which are complex particles that transport lipids (fats) in the bloodstream. These receptors play a crucial role in regulating the uptake and metabolism of lipids by cells, and are involved in a variety of physiological processes, including cholesterol homeostasis, inflammation, and insulin sensitivity. Dysregulation of lipoprotein receptors has been implicated in the development of a number of diseases, including atherosclerosis, type 2 diabetes, and metabolic syndrome.
List of immune cells
Karl Wilhelm von Kupffer
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Complement receptor of the immunoglobulin family
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Liver sinusoidal endothelial cell
Mononuclear phagocyte system
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Alcoholic liver disease
Hemochromatosis type 4
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MESH TREE NUMBER CHANGES - 2008 MeSH
- Although CD4 T cells are the main targets of HIV infection, macrophages also become infected and resist the cytopathic effects of infection, contributing potentially to HIV reservoir persistence. (nih.gov)
- these are liver-resident macrophages, or Kupffer cells, and lymphocytes, which process numerous antigens and pathogens from the gastrointestinal tract. (medpagetoday.com)
- Reticuloendothelial cells include macrophages in the bone marrow and spleen and Kupffer cells, which are specialized macrophages found in the liver that help protect the body against foreign invaders such as viruses and bacteria. (medlineplus.gov)
- A review on the relationship of mast cells and macrophages in breast cancer - Can herbs or natural products facilitate their anti-tumor effects? (spandidos-publications.com)
- Excess accumulation of cholesterol in macrophages results in foam cell production and lesion development. (jci.org)
- Hepatocytes and Kupffer cells are not affected. (medscape.com)
- Lobules are the functional units of the liver and consist of millions of cells called hepatocytes. (medicalnewstoday.com)
- Hepatocytes, as well as nonparenchymal cells, secrete proinflammatory cytokines and chemokines that are involved in the pathology of many liver diseases. (cdc.gov)
- Using human Hep G2 cells and freshly isolated rodent hepatocytes, it was demonstrated that metals increase gene expression and secretion of CXC chemokines and TNFalpha. (cdc.gov)
- Later in the course of the condition, iron also accumulates in liver cells (hepatocytes). (medlineplus.gov)
- The various functions of the liver are carried out by the liver cells, called hepatocytes, which act as stem cells and are responsible for the organ's unique ability to regenerate tissue. (oprah.com)
- 21). Colocalization research had been performed in liver organ areas from EtOH-treated dKO mice to determine whether 4-HNE adducts happened in Kupffer cells or stellate cells furthermore to hepatocytes. (eprf.ca)
- Moreover, primary cultured mouse hepatocytes exhibit much higher efficient copper exocytosis than primary cultured mouse Kupffer cells. (uri.edu)
- Hydrogen peroxide was used to induce an oxidative stress model of hepatocyte IAR-20 cells to evaluate the protective effects of BMMSCs in vitro. (medscimonit.com)
- Intravenous and intranasal pathogenicity tests the function of the PDZ-ligand domain otherwise present produced systemic disease with vascular endothelial cell at the C terminus of the NS1 protein ( 5 , 6 ). (cdc.gov)
- Since circulating cells in the liver are in contact predominantly with sinusoidal lining cells (Kupffer cells and endothelial cells), this postulate requires the presence of asialoglycoprotein receptors on the luminal surface of the sinusoidal lining cells. (nih.gov)
- The plasma membranes of Kupffer cells, endothelial cells, and fat-storing cells were devoid of the asialoglycoprotein receptor. (nih.gov)
- The term mononuclear phagocyte system has replaced the former reticuloendothelial system, which also included less active phagocytic cells such as fibroblasts and endothelial cells. (bvsalud.org)
- Lipid-poor HDL precursors mature by obtaining cholesterol and phospholipids from cell membranes or triglyceride-rich lipoproteins. (jci.org)
- Other sites of abnormal cell vacuolization include the renal glomerular podocytes and in the fibroblasts of the liver's periportal spaces. (medscape.com)
- Wherry and colleagues define the kinetics of vaccine-primed recall immune responses during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) breakthrough infection, highlighting rapid activation of memory T cells and broadly enhanced immune responses in previously vaccinated individuals. (nature.com)
- The concept that disease rooted principally in chronic aberrant constitutive and reactive activation of mast cells (MCs), without the gross MC neoplasia in mastocytosis, first emerged in the 1980s, but only in the last decade has recognition of "mast cell activation syndrome" (MCAS) grown significantly. (degruyter.com)
- Subsequent literature regarding this newly recognized (but of course not truly new) "mast cell activation syndrome" (MCAS) included case reports as well as formal studies (mostly relatively small scale), reviews, and various proposals for formal diagnostic criteria. (degruyter.com)
- 2017). Leishmania infantum exoproducts inhibit human invariant NKT cell expansion and activation . (up.pt)
- These findings demonstrate the central role lipid peroxidation plays in mediating progression of alcohol-induced necroinflammatory liver injury, stellate cell activation, matrix remodeling, and fibrosis. (eprf.ca)
- BMMSCs showed significant protective effects on the ultrastructure of DCD donor livers and ROS-induced injury to IAR-20 cells under electron microscopy. (medscimonit.com)
- To clarify this issue, we used an indirect immunoelectron microscopic method to determine the distribution of the receptor on the surfaces of hepatic cells accessible to the circulation. (nih.gov)
- In I-cell disease, the characteristic finding is abnormal vacuolization or inclusions that appear in the cytoplasm. (medscape.com)
- The histopathology was consistent with spontaneous splenic rupture, and showed the characteristic hemozoin pigment in the Kupffer cells. (ispub.com)
- Fig. 3: Histopathology showing characteristic malarial pigment in Kupffer cells. (ispub.com)
- 2017). Leishmania infantum antigens modulate memory cell subsets of liver resident T lymphocyte . (up.pt)
- Early enzymologic studies showed that cultured fibroblasts from patients with I-cell disease were deficient in numerous lysosomal enzymes. (medscape.com)
- I-cell disease fibroblasts were subsequently discovered to be able to internalize and use lysosomal enzymes produced by normal cells, whereas normal or other lysosomal disease fibroblasts were incapable of internalizing lysosomal enzymes secreted by the I-cell disease fibroblasts. (medscape.com)
- These are observed in cells of mesenchymal origin, especially fibroblasts. (medscape.com)
- The liver stores iron from hemoglobin in the form of ferritin, ready to make new red blood cells. (medicalnewstoday.com)
- Ferritin stores and releases iron in cells, and cells produce more ferritin in response to excess amounts of iron. (medlineplus.gov)
- BMMSCs also significantly improved the expression level of microtubule-associated protein 1 light chain 3 (LC3)-II in both DCD donor livers and ROS-induced injured IAR-20 cells, including upregulating the expression of ferritin. (medscimonit.com)
- It has been postulated that the selective accumulation of circulating desialylated cells in the mammalian liver results from the binding of desialylated glycoproteins on surfaces of the cells to asialoglycoprotein receptors in the liver. (nih.gov)
- Basal cells b. (histology-world.com)
- Basal cells d. (histology-world.com)
- intralobular duct of submandibular has striations at the basal surface of their cells. (brainscape.com)
- when you close condense, appears striated due to the parallel arrays of the mitochondria within the infolds of the plasma membrane at the basal surface of the cells. (brainscape.com)
- both mucous and serous cells that secrete into a common lumen. (brainscape.com)
- 2017). Leishmania infantum exerts immunomodulation in canine Kupffer cells reverted by meglumine antimoniate . (up.pt)
- To improve the quality of liver grafts from extended-criteria donors donated after circulatory death (DCD), this study explored whether bone marrow mesenchymal stem cells (BMMSCs) combined with normothermic machine perfusion (NMP) have protective effects on DCD donor livers and the effects of ferroptosis in this procedure. (medscimonit.com)
- In your liver, there are rows of liver cells separated by space. (oprah.com)
- Inhibitory effect of sodium houttuyfonate on synovial proliferation in vitro in cells from a patient with rheumatoid arthritis. (spandidos-publications.com)
- Here the authors use single cell profiling of T cells across the human lifespan to show that a suboptimal TCR shift in T cells as we enter older age results in a molecular signature that resembles that of T cells from newborns and children. (nature.com)
- The liver or bone marrow stores iron released from hemoglobin, which makes the next generation of blood cells. (medicalnewstoday.com)
- Bilirubin-it's a substance that comes from the breakup of hemoglobin in dead red blood cells. (oprah.com)
- Parameters checked: Packed cell volume (PCV), erythrocyte count (RBC), hemoglobin (Hgb), and total and differential leukocyte counts (WBC). (europa.eu)
- A report suggests that there is accumulation of inclusion bodies in B-cells of individuals with I-cell disease, which may imply impairment of the immune system. (medscape.com)
- Overview of Platelet Disorders Platelets are circulating cell fragments that function in the clotting system. (msdmanuals.com)
- what cell is this in the pancreas? (brainscape.com)
- Due to multiple valences of gold, redox reaction of gold within cells can increase the levels of reactive oxygen species (ROS), which interferes with the mitochondrial membrane potential. (uri.edu)
- Bio-Rad, Hercules, CA), (a Kupffer cell marker), or for the looks of -soft muscle tissue actin (-SMA) (Sigma, St. Louis, MO) (a marker of triggered stellate cells). (eprf.ca)
- possibly because the iron that accumulates in the liver, bone marrow, and spleen is less available for production of red blood cells. (medlineplus.gov)
- We were intrigued by experimental studies showing that in NAFLD many of these key immune cells become dysfunctional at various levels, which may affect disease progression and at the same time increase susceptibility to various viral, bacterial, and fungal infections. (medpagetoday.com)
- As in many of the lysosomal storage diseases, the functional deficiency of lysosomal enzymes results in abnormal cell architecture. (medscape.com)
- I-cell disease is an inherited lysosomal storage disorder. (medscape.com)
- thus, the disease was designated I-cell disease. (medscape.com)
- Profile view of 3-year-old with I-cell disease. (medscape.com)
- The biochemical defect in I-cell disease involves the first step in the addition of the mannose-6-phosphate moiety. (medscape.com)
- I-cell disease is a rare disorder that has no ethnic predilection. (medscape.com)
- You will find recent research articles and reviews that discuss the players and factors involved in stromal-immune cell interactions in both health and disease. (nature.com)
- I-cell disease has no racial predilection. (medscape.com)
- I-cell disease is inherited as an autosomal-recessive trait. (medscape.com)