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

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

Irritable bowel syndrome (IBS) is one of the most common functional gastrointestinal disorders and is that with the greatest socioeconomic impact worldwide. Diagnosis of IBS is based on clinical criteria that have been modified over time, the Rome II criteria being those that are currently followed. Some of the symptoms of IBS are similar to those in patients with inflammatory bowel disease (IBD), which can hamper or delay diagnosis. The use of inflammatory markers in stools (such as calprotectin) may help to distinguish between these two entities. A possible connection between IBS and IBD could be based on five points: (i) both disorders have similar symptoms; (ii) symptoms often overlap in the same patients; (iii) IBS and IBD have a common familial aggregation; (iv) some predisposing factors, such as a history of acute gastroenteritis, play a role in both disorders, and (v) importantly, signs of microinflammation are found in the bowels of patients with IBS. With regard to this latter point, an increase in inflammatory cells has been found in the intestinal mucosa of patients with IBS and, more specifically, mastocytes have been found to be increased in the jejunum and colon while CD3 and CD25 intraepithelial lymphocytes have be observed to be increased in the colon. Moreover, activated mastocytes are increased near to nerve endings in patients with IBS and this finding has been correlated with the intensity of both intestinal symptoms (abdominal pain) and psychological symptoms (depression and fatigue). A good model of microinflammation is post-infectious IBS, since the timing of the onset of the infectious process is known. In patients with post-infectious IBS, an increase in intraepithelial lymphocytes and enterochromaffin cells is initially found, which is reduced over time; consequently, although the symptoms of IBS persist, after 3 years no differences are detected in the number of inflammatory cells between IBS patients and controls. Among the various factors that can favor the development of IBS in these patients, two host-dependent mechanisms are most closely implicated in the physiopathology of IBS: polymorphism of the genes codifying pro- or anti-inflammatory cytokines and psychological factors such as anxiety, depression, somatization and neuroticism at the time of the acute infection. In view of all of the above, the similarities between IBS and IBD are probably more than mere coincidence and may reflect distinct manifestations of a broad spectrum of inflammation in the colon.
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PMID:[Irritable bowel syndrome and inflammatory bowel disease: Is there a connection?]. 1944 13

Children with acute RV-gastroenteritis (GE) had low or undetectable levels of circulating IFN-gamma(+), IL-13(+), IL-2(+), IL-10(+) or IL-17(+) RV-T cells. IFN-gamma(+) T cells and low frequencies of IL-10(+) and IL-2(+) CD4(+) T cells were found in adults with RV-GE during acute and convalescence phases, respectively. Circulating single IFN-gamma(+)>double IFN-gamma(+)/IL-2(+)>single IL-2(+)RV-CD4(+)T cells were observed in healthy adults. In this group, frequencies of IFN-gamma(+) RV-T cells increased after removing CD25(+)cells, blocking TGF-beta with its natural inhibitor, LAP, or inhibiting TGF-betaRI signalling pathway with ALK5i. The frequencies of IFN-gamma(+) RV-T cells were also incremented in PBMC depleted of CD25(+)cells and treated with ALK5i, suggesting that TGFbeta inhibition may be independent of Treg cells. The ALK5i effect was observed in adults but not in children with RV-GE, who had normal numbers of TGF-beta+ Treg cells. Thus, a TGF-beta-mediated regulatory mechanism that modulates RV-T cells in adults is not evident in children.
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PMID:A TGF-beta mediated regulatory mechanism modulates the T cell immune response to rotavirus in adults but not in children. 2009 11

Salmonella Typhimurium causes a self-limiting gastroenteritis that may lead to systemic disease. Bacteria invade the small intestine, crossing the intestinal epithelium from where they are transported to the mesenteric lymph nodes (MLNs) within migrating immune cells. MLNs are an important site at which the innate and adaptive immune responses converge but their architecture and function is severely disrupted during S. Typhimurium infection. To further understand host-pathogen interactions at this site, we used mass spectrometry imaging (MSI) to analyse MLN tissue from a murine model of S. Typhimurium infection. A molecule, identified as palmitoylcarnitine (PalC), was of particular interest due to its high abundance at loci of S. Typhimurium infection and MLN disruption. High levels of PalC localised to sites within the MLNs where B and T cells were absent and where the perimeter of CD169+ sub capsular sinus macrophages was disrupted. MLN cells cultured ex vivo and treated with PalC had reduced CD4+CD25+ T cells and an increased number of B220+CD19+ B cells. The reduction in CD4+CD25+ T cells was likely due to apoptosis driven by increased caspase-3/7 activity. These data indicate that PalC significantly alters the host response in the MLNs, acting as a decisive factor in infection outcome.
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PMID:Mass spectrometry imaging identifies palmitoylcarnitine as an immunological mediator during Salmonella Typhimurium infection. 2858 81