Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017160 (gastroenteritis)
 11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of orthotopic liver transplantation (OLTx) and cytomegalovirus (CMV) gastroenteritis on the type of mononuclear cells within the upper gastrointestinal tract were determined. Nineteen liver transplant recipients were studied both before and after transplantation. Each underwent a pan-upper gastrointestinal endoscopy with biopsy of the antrum and duodenum before and four weeks following liver transplantation. A panel of monoclonal antibodies prepared against HLA-DR, NK, IL-2R, T11, T4, T8, and B1 cell surface antigens was used to examine the tissues. Before OLTx, none of the 19 subjects studied had clinical or histologic evidence for CMV gastroenteritis. Following OLTx, five of the 19 subjects had CMV gastroenteritis. The number of HLA-DR positive staining lymphocytes present in biopsies obtained post-OLTx was significantly greater (P less than 0.005) than those present in biopsies obtained pre-OLTx regardless of the presence or absence of CMV gastroenteritis. No difference in the intensity of HLA-DR antigen expression between pre- and post-OLTx biopsies and those with and without CMV gastroenteritis was evident. No difference in the number of natural killer (NK) cells and the number of cells expressing the interleukin-2 receptor (IL-2R) was evident between biopsies obtained pre- and post-OLTx. In contrast, the number of T lymphocytes bearing the T11, T4, and T8 markers and the calculated T4/T8 ratio differed between biopsies obtained pre- and post-OLTx and between those positive for CMV gastroenteritis post-OLTx and those without evidence for CMV gastroenteritis either before or after OLTx, although these changes were not consistent throughout the gastrointestinal tract.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:T-lymphocyte subsets in gut and blood of liver transplant recipients with and without cytomegalovirus gastroenteritis. 255 22

During the fall of 1979, 22/250 Swedish UN soldiers serving in Egypt were hospitalized with fever and gastroenteritis associated with aseptic meningitis. One of the 22 developed insulin dependent diabetes mellitus (IDDM) 10 weeks following the infection. The majority of the 22 patients showed significant titer rise for coxsackievirus B by plaque reduction neutralization test. The serology results indicate that coxsackievirus B4 most likely caused the outbreak. All 22 were also tested for islet cell cytoplasmic antibodies and islet cell surface antibodies and found negative. The individual developing diabetes mellitus had the HLA-DR phenotype 3,4, which is associated with IDDM.
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PMID:An outbreak of coxsackievirus B infection followed by one case of diabetes mellitus. 298 80

Down-modulation of CD3zeta expression on CD8 T lymphocytes occurs, independently of other T-cell receptor (TCR)-CD3 components, in tumor-infiltrating lymphocytes, human immunodeficiency virus infection, and autoimmune disease. These associations suggest that it might be related to chronic antigenic stimulation. CD3zeta down-modulation was found, however, in CD8 T cells that proliferate in response to acute viral infections. In 3 otherwise healthy donors with acute gastroenteritis, infectious mononucleosis, and Epstein-Barr virus/cytomegalovirus/mononucleosis, 30% to 60% of circulating CD8 T cells had down-modulated CD3zeta to below the level of detection. The CD3zeta-T cells were also CD28- but expressed the activation markers HLA-DR and CD57. CD3zeta-CD28- T cells are effector CTL because they express perforin and produce IFN-gamma, but not IL-2, on activation and contain the viral-specific cytotoxic T lymphocyte (CTL). However, CD3zeta-CD28-T cells generally do not express CD25 after anti-CD3 and anti-CD28 stimulation and are not cytotoxic until they are cultured with IL-2 overnight. Cytotoxicity coincides with the re-expression of CD3zeta but not CD28. Down-modulation of CD3zeta and CD28 on effector CTL may control CTL triggering and proliferation to prevent immunopathogenesis.
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PMID:CD3zeta and CD28 down-modulation on CD8 T cells during viral infection. 1091 Sep 18

We describe a previously healthy boy who developed intestinal pseudo-obstruction following an episode of gastroenteritis at age 2 years. At presentation, the patient had mildly raised erythrocyte sedimentation rate and C-reactive protein level, and elevated antineutrophil cytoplasmic antibodies, antinuclear anti-DNA, and anti-smooth muscle antibodies. His electrogastrography was myopathic with no dominant frequency. First full-thickness intestinal biopsies showed a T lymphocytic myositis, particularly in the circular muscle. Steroid therapy resulted in clinical remission; cessation of steroids, in relapse. Further full-thickness biopsies showed an initial reduction in alpha-smooth muscle actin immunostaining in circular muscle myocytes and later atrophy and disappearance of many myocytes. Vascular and the remaining enteric smooth muscle cells showed HLA-DR and intercellular adhesion molecule 1 expression. These observations demonstrate the ability of enteric myocytes to take part in an inflammatory response and to change their phenotype, allowing them to act as antigen-presenting cells and to activate T cells. This and possible cytokine production by the myocytes play a role in their own destruction. This process responded to immunosuppressive therapy.
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PMID:Acquired myopathic intestinal pseudo-obstruction may be due to autoimmune enteric leiomyositis. 1191 Mar 63