Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022104 (irritable bowel syndrome)
 8,033 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Scid mice develop a severe, chronic, and lethal IBD 3-6 months after engraftment of gut wall from immunocompetent congenic donors, induced by donor-derived CD4+ T cells migrating from the graft. We have investigated intracellular T-helper type 1 (Th1) cytokines in the spleens of gut wall-transplanted scid mice with IBD. Increased fractions of interferon-gamma (IFN-gamma), tumour necrosis factor-alpha (TNF-alpha) and IL-2-positive CD4+ T cells were found in the spleens of diseased mice compared with control mice. Moreover, a small but significant population of CD4+ T cells which stained positive for granulocyte-macrophage colony-stimulating factor (GM-CSF) was found in scid mice with IBD but was virtually absent in congenic non-scid control mice. Cloning of granulocyte/ macrophage colony-forming cells (G/M-CFC) revealed that both non-transplanted scid mice and scid mice with IBD had an 8-14-fold increase in splenic G/M-CFC compared with control mice. No significant difference in the number of G/M-CFC per total spleen was found between non-transplanted and disease scid mice, although both groups of mice showed a nearly two-fold increase compared with control mice. G/M-CFC were never found in the thymus, liver or lymph nodes of diseased mice. Immunohistochemistry revealed that the multinucleated giant cells observed in the gut wall of diseased mice did not represent haematopoietic foci, but were derived from macrophages. These observations point towards a dominant role for Th1-type CD4+ T cells in the immunopathogenesis of IBD, whereas haematopoiesis does not seem to be affected by the development of the disease.
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PMID:Splenic T helper cell type 1 cytokine profile and extramedullary haematopoiesis in severe combined immunodeficient (scid) mice with inflammatory bowel disease (IBD). 947 77

Eosinophilic gastroenteritis is a rare gastrointestinal (GI) disorder of undetermined cause characterized by infiltration of eosinophils in the GI tract. Eosinophils accumulate in tissues and may release highly cytotoxic granular proteins, which cause severe tissue damage characteristic of eosinophilic gastroenteritis. Eotaxin may play a role in the recruitment of eosinophils into tissue in combination with chemoattractants and cytokines, including interleukin 3 and 5 and granulocyte-macrophage colony-stimulating factor. Food allergy, especially in children, can be a triggering factor, and an amino acid-based diet may be helpful. Accumulation of eosinophils in the gut is a common feature in food-induced GI disorders that can be regulated through a complex molecular network involving Th2 cells, various cytokines, and chemokines. Eosinophilic gastroenteritis has a wide spectrum of clinical presentation depending on the site of involvement. It may be confused with irritable bowel syndrome or dyspepsia and, rarely, mimics pancreatitis or appendicitis. Diagnosis is important and is usually made by a pathologist. Eosinophilic gastroenteritis is a treatable disease; patients generally respond to steroid therapy, although relapse is common. Non-enteric-coated budesonide, a locally acting corticosteroid with little risk of adrenal suppression, may be substituted, although more experience is needed. Promising new drugs for eosinophilic gastroenteritis include montelukast, a selective leukotriene receptor antagonist, and suplaplast tosilate, a selective Th2 cytokine inhibitor with inhibitory effects on allergy-induced eosinophilic infiltration and IgE production. Although it is likely a separate disease, more experience has accumulated, and an elimination or specific amino acid-based diet appears to be helpful in treatment.
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PMID:Eosinophilic gastroenteritis. 1222 38

Luteolin (3',4',5,7-tetrahydroxylflavone) is a plant flavonoid and pharmacologically active agent that has been isolated from several plant species. In the present study, the effect of luteolin from the flowers of Lonicera japonica on phorbol 12-myristate 13-acetate (PMA) plus A23187-induced mast cell activation was examined. Luteolin significantly inhibited the induction of inflammatory cytokines such as tumor necrosis factor (TNF)-alpha, interleukin (IL)-8, IL-6 and granulocyte-macrophage colony-stimulating factor (GM-CSF) by PMA plus A23187. Moreover, luteolin attenuated cyclooxygenase (COX)-2 expression and intracellular Ca2+ levels. In activated HMC-1 cells, the phosphorylation of extra-signal response kinase (ERK 1/2) and c-jun N-terminal Kinase (JNK 1/2), but not p38 mitogen-activated protein kinase (p38 MAPK) were decreased by treatment of the cells with luteolin. Luteolin inhibited PMA plus A23187-induced nuclear factor (NF)-kappaB activation, IkappaB degradation, and luciferase activity. Furthermore, luteolin suppressed the expression of TNF-alpha, IL-8, IL-6, GM-CSF, and COX-2 through a decrease in the intracellular Ca2+ levels, and also showed a suppression of the ERK 1/2, JNK 1/2, and NF-kappaB activation. These results indicated that luteolin from the flowers of Lonicera japonica exerted a regulatory effect on mast cell-mediated inflammatory diseases, such as RA, allergy disease and IBD.
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PMID:Luteolin isolated from the flowers of Lonicera japonica suppresses inflammatory mediator release by blocking NF-kappaB and MAPKs activation pathways in HMC-1 cells. 2011 Aug 98