Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085110 (SCID)
 11,041 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Escherichia coli strain Nissle 1917 (EcN) is as effective in maintaining remission in ulcerative colitis as is treatment with mesalazine. This study aims to evaluate murine models of acute and chronic intestinal inflammation to study the antiinflammatory effect of EcN in vivo. Acute colitis was induced in mice with 2% dextran-sodium sulfate (DSS) in drinking water. EcN was administered from day -2 to day +7. Chronic colitis was induced by transfer of CD4(+) CD62L(+) T lymphocytes from BALB/c mice in SCID mice. EcN was administered three times/week from week 1 to week 8 after cell transfer. Mesenteric lymph node (MLN) cytokine secretion (of gamma interferon [IFN-gamma], interleukin 5 [IL-5], IL-6, and IL-10) was measured by enzyme-linked immunosorbent assay. Histologic sections of the colon were analyzed by using a score system ranging from 0 to 4. Intestinal contents and homogenized MLN were cultured, and the number of E. coli-like colonies was determined. EcN was identified by repetitive extragenic palindromic (REP) PCR. EcN administration to DSS-treated mice reduced the secretion of proinflammatory cytokines (IFN-gamma, 32,477 +/- 6,377 versus 9,734 +/- 1,717 [P = 0.004]; IL-6, 231 +/- 35 versus 121 +/- 17 [P = 0.02]) but had no effect on the mucosal inflammation. In the chronic experimental colitis of the transfer model, EcN ameliorated the intestinal inflammation (histology score, 2.7 +/- 0.2 versus 1.9 +/- 0.3 [P = 0.02]) and reduced the secretion of proinflammatory cytokines. Translocation of EcN and resident E. coli into MLN was observed in the chronic colitis model but not in healthy controls. Administration of EcN ameliorated acute and chronic experimental colitis by modifying proinflammatory cytokine secretion but had no influence on the acute DSS-induced colitis. In this model, preexisting colitis was necessary for translocation of EcN and resident E. coli into MLN.
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PMID:Preventive effects of Escherichia coli strain Nissle 1917 on acute and chronic intestinal inflammation in two different murine models of colitis. 1501 90

Apoptosis is a programmed physiological death of unwanted cells, and handling of apoptotic cells (ACs) is thought to have profound effects on immune-mediated disorders. However, there is scant information regarding the role of ACs in intestinal inflammation, in which immune homeostasis is a major concern. To investigate this, we injected ACs into a severe combined immunodeficiency adoptive transfer model of chronic colitis in the presence and absence of cotransferred whole B or regulatory B cell (Breg)-depleted B cells. We also injected syngeneic ACs into AKR/N mice as a control and into milk fat globule-epidermal growth factor 8 knockout mice deficient of phagocytic function. Chronic colitis severity was significantly reduced in the AC as opposed to the phosphate-buffered saline group with cotransferred whole B cells. The AC-mediated effect was lost in the absence of B cells or presence of Breg-depleted B cells. In addition, ACs induced splenic B cells to secrete significantly increased levels of interleukin 10 in AKR/N mice but not milk fat globule-epidermal growth factor 8 knockout mice. Apoptotic leukocytes were induced by reactive oxygen species during granulocyte/monocyte apheresis therapy in rabbits and H2O2-induced apoptotic neutrophils ameliorated mice colitis. Our results indicate that ACs are protective only in the presence of B cells and phagocytosis of ACs induced interleukin 10 producing Bregs. Thus, the ameliorative effect seen in this study might have been exerted by AC-induced Bregs through increased production of the immunosuppressive cytokine interleukin 10, whereas an AC-mediated effect may contribute to the anti-inflammatory effect of granulocyte/monocyte apheresis as a novel therapeutic mechanism for inflammatory bowel disease.
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PMID:Apoptotic cells ameliorate chronic intestinal inflammation by enhancing regulatory B-cell function. 2535 66