Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021831 (enteropathy)
 4,403 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have investigated the role of interferon-alpha/beta (IFN-alpha/beta) and IFN-dependent effector cells in causing enteropathy in mice. The IFN-inducer polyinosinic:polycytydylic acid (poly I:C) augmented the natural killer (NK) cell activation normally seen in neonatal (CBA x BALB/c)F1 mice with graft-versus-host reaction (GVHR) and exacerbated the systemic and intestinal consequences of GVHR. Poly I:C itself produced a similar pattern of intestinal pathology when administered to normal mice. The effects of poly I:C on NK cell activity and intestinal architecture in normal mice could be reproduced by a single injection of purified IFN-alpha/beta and the intestinal lesions caused by IFN-alpha/beta were prevented by in vivo depletion of NK cells with anti-asialo GM1. These results indicate that IFN-alpha/beta may play an important role in immunologically mediated enteropathies by virtue of its ability to activate NK cells.
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PMID:The role of interferon alpha/beta in the induction of intestinal pathology in mice. 174 74

We have shown previously that normal mice given interferon-alpha/beta (IFN-alpha/beta) or tumour necrosis factor-alpha (TNF-alpha) develop marked intestinal pathology which is similar to that found in enteropathies associated with cell-mediated immunity in vivo, such as graft-versus-host reaction (GVHR). The enteropathy induced by IFN-alpha/beta and GVHR are both dependent on the presence of natural killer (NK) cells and here we have examined whether NK cells are also required for enteropathy caused by TNF-alpha. Mice injected with recombinant TNF-alpha displayed enhanced splenic NK cell activity and developed significant villus atrophy and crypt hypertrophy in the small intestine. Administration of anti-asialo GM1 antibody abolished the NK cell activity in both normal and TNF-alpha-injected mice, but had no effect on the enteropathy caused by TNF-alpha. We conclude that NK cells are not required for TNF-alpha to damage the small intestine.
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PMID:Natural killer cells and tumour necrosis factor-alpha-mediated enteropathy in mice. 847 22

INTRODUCTION Celiac disease (CD) is an immune-mediated enteropathy related to permanent gluten intolerance, characterized by gastrointestinal symptoms as well as nongastrointestinal symptoms, including neurologic ones. The presence of neuron-specific enolase (NSE), interleukin 10 (IL-10), and antiganglioside M1 (anti-GM1) antibodies has been demonstrated for neurologic conditions as well as immune disorders with neurologic manifestations. OBJECTIVES The aim of the study was to determine the concentrations of IL-10, NSE, and anti-GM1 antibodies in the course of CD and their correlation with changes in electrogastrography (EGG) and with heart rate variability (HRV). PATIENTS AND METHODS The study included 68 participants: 34 patients with CD and 34 healthy individuals. We assessed the concentrations of IL-10 and NSE as well as the presence of anti-GM1 antibodies in serum. We investigated correlations between the concentrations of IL-10, NSE, and anti-GM1 antibodies and the results of EGG and HRV. RESULTS Patients with CD had a higher level of anti-GM1 antibodies than controls (1.38 ng/ml [0.98-2.03 ng/ml] vs 0.81 ng/ml [0.35-1.15 ng/ml]). Median IL-10 concentrations in patients with CD differed significantly from those in controls (7 pg/ml [4.33-11.48 pg/ml] vs 4.27 pg/ml [2.44-7 pg/ml]; P = 0.010). In HRV analysis, a positive correlation between IL-10 concentrations and very low frequency spectrum was observed (r = 0.63; P = 0.003). There was no correlation between the concentrations of IL-10, NSE, or anti-GM1 antibodies and EGG parameters. CONCLUSIONS Chronic inflammation in the course of CD may lead to autonomic nervous system impairment and development of neurologic disorders. Therefore, anti-GM1 antibodies and IL-10 may be considered as markers of nervous system impairment in the course of CD.
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PMID:Concentrations of antiganglioside M1 antibodies, neuron-specific enolase, and interleukin 10 as potential markers of autonomic nervous system impairment in celiac disease. 2790 75