Agriculture and Agri-Food Canada, Lethbridge, Canada.
Am J Physiol Gastrointest Liver Physiol. 2010 Jan;298(1):G1-9. doi: 10.1152/ajpgi.00193.2009. Epub 2009 Oct 29.
The inflammatory bowel diseases (IBD), Crohn's disease and ulcerative colitis, are T cell-mediated diseases that are characterized by chronic, relapsing inflammation of the intestinal tract. The pathogenesis of IBD involves the complex interaction between the intestinal microflora, host genetic and immune factors, and environmental stimuli. Epidemiological analyses have implicated acute bacterial enteritis as one of the factors that may incite or exacerbate IBD in susceptible individuals. In this review, we examine how interactions between the common enteric pathogen Campylobacter jejuni (C. jejuni), the host intestinal epithelium, and resident intestinal microflora may contribute to the pathogenesis of IBD. Recent experimental evidence indicates that C. jejuni may permit the translocation of normal, noninvasive microflora via novel processes that implicate epithelial lipid rafts. This breach in intestinal barrier function may, in turn, prime the intestine for chronic inflammatory responses in susceptible individuals. Insights into the interactions between enteric pathogens, the host epithelia, and intestinal microflora will improve our understanding of disease processes that may initiate and/or exacerbate intestinal inflammation in patients with IBD and provide impetus for the development of new therapeutic approaches for the treatment of IBD.
炎症性肠病（IBD），包括克罗恩病和溃疡性结肠炎，是由 T 细胞介导的疾病，其特征是肠道慢性、复发性炎症。IBD 的发病机制涉及肠道微生物群、宿主遗传和免疫因素以及环境刺激之间的复杂相互作用。流行病学分析表明，急性细菌性肠炎是可能在易感个体中引发或加重 IBD 的因素之一。在这篇综述中，我们研究了常见肠道病原体空肠弯曲菌（C. jejuni）、宿主肠道上皮细胞和常驻肠道微生物群之间的相互作用如何有助于 IBD 的发病机制。最近的实验证据表明，C. jejuni 可能通过涉及上皮脂筏的新过程允许正常、非侵入性微生物群的易位。这种肠道屏障功能的破坏反过来可能使易感个体的肠道对慢性炎症反应产生致敏作用。深入了解肠道病原体、宿主上皮细胞和肠道微生物群之间的相互作用将提高我们对可能引发和/或加重 IBD 患者肠道炎症的疾病过程的理解，并为治疗 IBD 的新治疗方法的发展提供动力。
