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Increased incidence of inflammatory bowel disease: the price of the decline of infectious burden?

机译:炎性肠病的发病率上升:传染病负担下降的代价?

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摘要

PURPOSE OF REVIEW: It is now apparent that the increase in the incidence of autoimmune and allergic diseases in Western countries is explained by the decrease in infections. The question is posed to determine whether a similar explanation can be proposed for the increased incidence of inflammatory bowel disease. RECENT FINDINGS: Studies performed in murine experimental models of inflammatory bowel disease have shown that colitis onset can be prevented by bacteria, bacterial extracts, or helminths. Particular interest was given to probiotics (either live or killed), which protect from disease in a toll-like receptor 9 dependent fashion. This protective effect involves regulatory cytokines as indicated by in vitro studies on human inflamed colonic cells. At the clinical level, there is strong suggestion but still limited proof that probiotics improve inflammatory bowel disease through immunoregulatory mechanisms. SUMMARY: Converging clinical and experimental data strongly suggest the protective nonspecific role of infections on inflammatory bowel disease independently from the triggering role of some specific bacteria. The extension to inflammatory bowel disease of the hygiene hypothesis opens new therapeutic perspectives including the revisiting of probiotics and other forms of exposure to bacteria or parasite components.
机译:审查目的:显而易见,西方国家自身免疫性疾病和过敏性疾病的发生率增加是由于感染减少所致。提出这个问题是为了确定是否可以为炎症性肠病的增加发病率提出类似的解释。最近的发现:在小鼠炎症性肠病实验模型中进行的研究表明,细菌,细菌提取物或蠕虫可以预防结肠炎的发作。益生菌(无论是活的还是被杀死的)特别令人关注,它们以收费类似的受体9依赖性方式预防疾病。如对人发炎的结肠细胞的体外研究所表明的,这种保护作用涉及调节性细胞因子。在临床上,有强烈的建议,但仍然有限的证据表明益生菌可通过免疫调节机制改善炎症性肠病。摘要:临床和实验数据的融合强烈表明感染对炎症性肠病的保护性非特异性作用独立于某些特定细菌的触发作用。卫生学假说对炎症性肠病的扩展开辟了新的治疗前景,包括重新审视益生菌和其他形式的细菌或寄生虫成分暴露。

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