Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

CD1d is a major histocompatibility complex (MHC) class I-related molecule that functions in glycolipid antigen presentation to distinct subsets of T cells that express natural killer receptors and an invariant T-cell receptor-alpha chain (invariant NKT cells). The acquisition of glycolipid antigens by CD1d occurs, in part, in endosomes through the function of resident lipid transfer proteins, namely saposins. Here we show that microsomal triglyceride transfer protein (MTP), a protein that resides in the endoplasmic reticulum of hepatocytes and intestinal epithelial cells (IECs) and is essential for lipidation of apolipoprotein B, associates with CD1d in hepatocytes. Hepatocytes from animals in which Mttp (the gene encoding MTP) has been conditionally deleted, and IECs in which Mttp gene products have been silenced, are unable to activate invariant NKT cells. Conditional deletion of the Mttp gene in hepatocytes is associated with a redistribution of CD1d expression, and Mttp-deleted mice are resistant to immunopathologies associated with invariant NKT cell-mediated hepatitis and colitis. These studies indicate that the CD1d-regulating function of MTP in the endoplasmic reticulum is complementary to that of the saposins in endosomes in vivo.
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PMID:CD1d function is regulated by microsomal triglyceride transfer protein. 1510 43

Interleukin 18 has been known since 1989 and since its properties have been recognized, an interest in it is constantly growing. IL-18 induces synthesis and release of proinflammatory cytokines, chemokines and nitric oxide. Thus, it modulates the function of many immunocompetent cells: macrophages, monocytes, lymphocytes and granulocytes. In the paper, properties of IL-18 are reviewed and its implications for pathogenesis of some gastrointestinal diseases, particularly inflammatory bowel diseases, i.e. Crohn Disease and colitis ulcerosa, inflammatory liver diseases such as persistent active hepatitis and primary biliary cirrhosis and acute pancreatitis are discussed.
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PMID:[Interleukin 18 as a new immunomodulator of some digestive tract diseases]. 1519 Jun 10

Human cytomegalovirus is a large DNA virus that is well-equipped to evade both innate and adaptive host immune responses and to establish lifelong latency. It is a major opportunistic pathogen in immunocompromised hosts. Following allogeneic transplantation, immune responses are often inadequate to inhibit viral reactivation, resulting in progressive tissue damage, manifesting as overt human cytomegalovirus disease that usually presents as pneumonitis, colitis or hepatitis. Currently available antiviral pharmacotherapies are limited by toxicities if used prophylactically, and by a lack of efficacy in established human cytomegalovirus disease. Efforts have therefore focused on molecular diagnostic surveillance protocols that allow earlier intervention and the development of adoptive immunotherapeutic strategies to hasten host immune reconstitution.
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PMID:Cytomegalovirus following stem cell transplantation: from pharmacologic to immunologic therapy. 1548 20

The idiopathic hypereosinophilic syndrome (HES) developed in a 15-year-old boy who presented with colitis, cough, rash, and hepatitis. Molecular analysis failed to demonstrate the Fip1-like1-Platelet Derived Growth Factor Receptor alpha chain (FIP1L1-PDGFRA) mutation described in adult patients with HES. There are significant clinical differences between the pediatric and adult presentations of HES.
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PMID:Pediatric hypereosinophilic syndrome (HES) differs from adult HES. 1635 54

Macrophage migration inhibitory factor (MIF) is a unique protein, participating in inflammation, immune response, and cell growth. MIF was first discovered as a lymphokine involved in delayed hypersensitivity and various macrophage functions, including phagocytosis, spreading, and tumoricidal activity. It has been reported that MIF is associated with the pathogenesis of a variety of diseases. MIF expression was increased at inflammatory sites in diseases such as rheumatoid arthritis and glomerulonephritis. In experimental inflammatory disease, blockade of MIF bioactivity inhibited the severity of disease activity. On the other hand, MIF expression is also increased in tumor lesions, and MIF plays a role as a cell growth factor. MIF has been reported to be constitutively expressed in gut, liver, and pancreas. In patients with gastritis, inflammatory bowel disease, hepatitis, and pancreatitis, MIF expression was remarkably increased in both the serum and the local lesions. Blockade of MIF bioactivity inhibited and prevented inflammation in experimental gastritis, colitis, hepatitis, and pancreatitis. On the other hand, MIF expression was higher than that in normal tissues in colonic carcinomas and hepatocellular carcinoma both in vivo and in vitro. Blockade of MIF bioactivity successfully inhibited tumor cell growth in vivo and in vitro. MIF plays important roles in the pathogenesis of gastrointestinal, hepatic, and pancreatic disorders.
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PMID:Pathophysiological roles of macrophage migration inhibitory factor in gastrointestinal, hepatic, and pancreatic disorders. 1577 Mar 93

Cytomegalovirus (CMV) causes infections in healthy individuals and compromised hosts. In compromised hosts, CMV may cause encephalitis, pneumonia, hepatitis, colitis, and so forth. In immunocompetent hosts, CMV mononucleosis is the most common clinical manifestation and CMV colitis is rare. We present a case of an 82-year-old immunocompetent man who presented with community-acquired bloody diarrhea. A computed tomography scan of the abdomen revealed pan-colitis. His age and abdominal pains suggested ischemic colitis as the cause of his bloody diarrhea. Workup for Clostridium difficile and all enteric pathogens were negative. The patient remained febrile with abdominal pain. During the second week, he underwent sigmoidoscopy for biopsy, which revealed viral inclusions of the Cowdry owl eye inclusion bodies characteristic of CMV. CMV colitis was diagnosed in the patient; he was successfully treated with a course of oral valganciclovir and made an uneventful recovery.
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PMID:Cytomegalovirus colitis mimicking ischemic colitis in an immunocompetent host. 1602 52

The role of leptin in the immune system has been well established. While adipocytes represent the major source, leptin production by lymphocytes, infiltrating at the site of inflammation, was recently demonstrated. However, the significance of this locally released leptin remains unresolved. In the present study, two models in which absence of leptin-signalling is associated with protection were employed: the model of ConA-induced hepatitis and the CD4(+)CD45Rb(high) transfer model of colitis. For the ConA model, scid mice were reconstituted with either WT or leptin-deficient (ob/ob) CD4(+) T cells. Eight weeks post transfer, ConA was injected and serum ALT, TNFalpha, leptin as well as liver mononuclear cell activation and histological signs of inflammation were evaluated. No difference between recipients of WT or ob/ob cells was observed for any of the parameters evaluated. In the second model, either WT or ob/ob CD4(+)CD45Rb(high) cells were transferred into scid mice. No histological differences were detected, although recipients of ob/ob cells showed higher weight loss compared to recipients of WT cells. Spontaneous production of IL-6 from colon cultures obtained from recipients of ob/ob cells was reduced compared to recipients of WT cells, whereas stimulation of lamina propria lymphocytes with leptin resulted in a higher IFNgamma release in recipients of ob/ob cells compared to recipients of WT cells. In conclusion, the present study provides evidence that T cell-derived leptin does not play a major role in the regulation of the inflammatory process, indicating that the adipose tissue is the critical player in the immune-modulating effects of leptin.
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PMID:Defining the role of T cell-derived leptin in the modulation of hepatic or intestinal inflammation in mice. 1617 53

Selective inhibitors of cyclooxygenase-2 have less gastroduodenal toxicity than non selective anti-inflammatory drugs. However, there is little information on their effect on the distal gut. A 91 year old woman presented with acute diarrhoea 5 weeks after beginning celecoxib treatment. Laboratory results showed an inflammatory syndrome and increased alanine aminotransferase (ALT) to 13 N. Endoscopic examination of the colon showed diffuse erythematous lesions of the sigmoid and of part of the right colon. No aetiology has been found for colitis or hepatitis. Diarrhea and blood test anomalies disappeared one week after celecoxib was stopped. The role of celecoxib in the etiology of colitis was considered plausible but not for liver damage. This report and a few other cases in the literature suggest that cyclooxygenase-2 selective non-steroidal anti-inflammatory drug inhibitor toxicity should be investigated in case of unexplained acute colitis.
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PMID:[Acute colitis closely following the beginning of celecoxib treatment]. 1651 92

Autoimmune hepatitis is a rare, chronic inflammatory disorder which has been associated with a number of other auto-immune conditions. However, there are no reports in the medical literature of an association with microscopic (lymphocytic) colitis. We report the case of a 53-year-old woman with several autoimmune conditions, including lymphocytic colitis, who presented with an acute hepatitis. On the basis of the clinical features, serology, and histopathology, we diagnosed autoimmune hepatitis. To our knowledge, this is the first report of autoimmune hepatitis in association with lymphocytic colitis, and lends support to the theory of an autoimmune etiology for lymphocytic colitis.
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PMID:Autoimmune hepatitis in association with lymphocytic colitis. 1691 12

Under immunosuppressive conditions after hematopoietic stem cell transplantation (HSCT), even if hepatitis B virus (HBV) antigen is negative but hepatitis B surface antibody (HBsAb) or hepatitis B core antibody (HBcAb) is presented, HBV reactivates and sometimes causes fulminant hepatitis. However, it remains unclear which patients will develop fulminant hepatitis, or whether fulminant hepatitis is caused by host-related factors or by virus-related factors. A 30-yr-old man with a history of aplastic anemia since 3 yr of age underwent allogenic BMT, when HBsAb and HBcAb were positive but HBs antigen (HBsAg) was negative. The donor was negative for HBsAg, HBsAb and HBcAb. After transplantation, the patient was complicated by acute graft-vs.-host disease (GVHD), cytomegalovirus infection, intestinal thrombotic microangiopathy and aspergillus colitis. Chronic GVHD was well controlled by FK506 and prednisolone. Twenty months after transplantation, the patient was admitted with general fatigue and liver dysfunction and was found to be positive for HBsAg and HBeAg. His serum HBV-DNA level was >8.8 log of the genome equivalent (LGE)/mL. Therefore, he was diagnosed as having hepatitis B caused by HBV reactivation and 100 mg/d lamivudine treatment was started. However, jaundice and hepatic failure deteriorated and became fatal. On analysis of the HBV-DNA, two adjacent gene mutations in the core promoter region (T1762/A1764) were detected. Increased replication of the mutated HBV might have caused HBV reactivation which progressed to fulminant hepatitis.
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PMID:Fulminant hepatitis after allogenic bone marrow transplantation caused by reactivation of hepatitis B virus with gene mutations in the core promotor region. 1692 12


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