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Intestinal Immune Responses (intestinal + immune_response)
Selected AbstractsThe mucosal immune systemPARASITE IMMUNOLOGY, Issue 5 2003Thomas T. MacDonald SUMMARY This article outlines the lymphoid structures and cell types important in the intestinal immune response. Particular attention is paid to differences between rodents and man where there appears to be fundamental differences in the sources of the T and B cells which populate the mucosa. The majority of the data still suggest that Peyer's patches are the inductive site of mucosal immunity and the mucosa (lamina propria and epithelium) is the effector site, but there is growing realization that mucosal immune responses can occur in the absence of Peyer's patches and that antigen sampling may also occur in the lamina propria. [source] Health-beneficial effects of probiotics: Its mode of actionANIMAL SCIENCE JOURNAL, Issue 4 2009Yuji OHASHI ABSTRACT It is now widely recognized that probiotics have health-beneficial effects on humans and animals. Probiotics should survive in the intestinal tract to exert beneficial effects on the host's health. To keep a sufficient level of probiotic bacteria in the gastrointestinal tract, a shorter interval between doses may be required. Although adherence to the intestinal epithelial cell and mucus is not a universal property of probiotics, high ability to adhere to the intestinal surface might strongly interfere with infection of pathogenic bacteria and regulate the immune system. The administration of probiotic Lactobacillus stimulated indigenous Lactobacilli and the production of short-chain fatty acids. This alteration of the intestinal environment should contribute to maintain the host's health. The immunomodulatory effects of probiotics are related to important parts of their beneficial effects. Probiotics may modulate the intestinal immune response through the stimulation of certain cytokine and IgA secretion in intestinal mucosa. The health-beneficial effects, in particular the immunomodulation effect, of probiotics depend on the strain used. Differences in indigenous intestinal microflora significantly alter the magnitude of the effects of a probiotic. Specific probiotic strains suitable for each animal species and their life stage as well as each individual should be found. [source] Defective arachidonate release and PGE2 production in Gi,2-deficient intestinal and colonic subepithelial myofibroblastsINFLAMMATORY BOWEL DISEASES, Issue 3 2006Robert Andrew Edwards MD Abstract Background: Mice lacking the pertussis toxin-sensitive G-protein subunit Gi,2 spontaneously develop colitis and colon cancer. In the gut, arachidonate-derived prostaglandin E2 (PGE2) modulates intestinal immune responses and epithelial restitution and is derived largely from subepithelial myofibroblasts. Methods: We tested whether known decreases in arachidonate release in cells lacking Gi,2 would result in decreased PGE2 production and tissue PGE2 levels. PGE2 levels were significantly decreased in the colon of Gi,2,/, mice. Results: Gi,2,/, myofibroblasts from the small intestine and colon both released ,50% less arachidonate and 3- to 7-fold less PGE2 and 6-keto PGF1, in response to adenosine triphosphate, thrombin, tumor necrosis factor-,, or lipopolysaccharide, in a partially cyclooxygenase (COX)-2-dependent manner. Decreased arachidonate release did not appear to be caused by a defect in cPLA2 translocation in the absence of Gi,2. Basal myofibroblast COX-1 and COX-2 expression was downregulated in Gi,2,/, cells. No differences in proliferation rates were found between serum-starved or serum-activated wild-type (WT) and Gi,2,/, myofibroblasts. Finally, treatment of Gi,2,/, mice with the EP4 -specific PGE2 receptor agonist ONO-AE1-329 significantly decreased the severity of established colitis. Conclusions: These findings confirm a requirement for Gi,2 in intestinal and colonic myofibroblast-derived prostanoid production and confirm the importance of mucosal PGE2 in the suppression of colitis. [source] Bacterial regulation of intestinal immune responsesINFLAMMATORY BOWEL DISEASES, Issue 2 2000Dr. Thomas T. MacDonald First page of article [source] Gene expression in distal intestine of Atlantic salmon (Salmo salar L.) fed genetically modified soybean mealAQUACULTURE NUTRITION, Issue 3 2008M.K. FRØYSTAD Abstract Limited availability of fishmeal leads to exploration of alternative protein sources like soybean meal (SBM). During the last decade, genetically modified (GM) plants have been introduced to the production of soybean crops. In the current experiment RNA was isolated from the distal intestinal section of Atlantic salmon fed either GM SBM or its near-isogenic parental line (non-GM), both at 30% inclusion. From a suppression subtractive hybridization cDNA library, 95 clones were sequenced. Clones with similarity to both known Atlantic salmon genes and novel Atlantic salmon sequences were identified. Real-time polymerase chain reaction was used to study differential expression of seven clones between the dietary groups. The clones were selected based on their relevance to intestinal immune responses and nutrient metabolism. Expression of a serum lectin-like clone was down-regulated in the GM group compared with the non-GM group. No differential expression was observed for six other clones with similarity to actin-related protein 2/3 complex-subunit 3, cysteine-rich intestinal protein, fatty acid binding protein/gastrotropin, ferritin heavy subunit, anterior gradient protein and peptide transporter. In conclusion, only minor differences in distal intestine transcriptional gene expression were observed between fish fed the diets with the non-GM and GM varieties. [source] |