Ellermann Melissa, Sartor R Balfour
Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Departments of Medicine, University of North Carolina, Chapel Hill, NC, USA.
J Immunol Sci. 2018;2(2):13-18.
Host-associated microbial communities modulate numerous aspects of host physiology at the epithelial interface within mucosal environments. Perturbations to this symbiotic relationship between host and microbiota has been linked to numerous microbial-driven pathological states, including Crohn's disease (CD). This is in part driven by the outgrowth of aggressive resident bacterial strains such as adherent and invasive Escherichia coli (AIEC) and changes in bacterial physiology and function that promote enhanced mucosal association of pathobionts and aberrant stimulation of mucosal immunity. Endogenous bacteria from host-associated microbial communities can adopt a sessile lifestyle and form multicellular structures known as biofilms that are generated through the expression of extracellular adhesion factors that include curli amyloid fibrils, cellulose and type 1 pili. In addition to enabling bacterial attachment to mucosal surfaces, biofilm components also stimulate immune responses and can therefore instigate or perpetuate microbial-driven inflammatory diseases such as CD. These host-bacterial interactions provide pharmacological targets that can potentially be exploited to limit mucosal adherence of aggressive enteric bacteria, inappropriate stimulation of inflammatory immune responses and consequent development of chronic intestinal inflammation.
宿主相关的微生物群落可调节黏膜环境中上皮界面处宿主生理的多个方面。宿主与微生物群之间这种共生关系的紊乱与多种微生物驱动的病理状态有关，包括克罗恩病（CD）。部分原因是诸如黏附侵袭性大肠杆菌（AIEC）等具侵袭性的常驻细菌菌株的增殖，以及细菌生理和功能的变化，这些变化促进了致病共生菌与黏膜的更强关联以及对黏膜免疫的异常刺激。宿主相关微生物群落中的内源细菌可采取固着生活方式并形成称为生物膜的多细胞结构，生物膜通过包括卷曲淀粉样纤维、纤维素和1型菌毛在内的细胞外黏附因子的表达而产生。除了使细菌能够附着于黏膜表面外，生物膜成分还会刺激免疫反应，因此可引发或延续诸如CD等微生物驱动的炎症性疾病。这些宿主与细菌之间的相互作用提供了潜在可被利用的药理学靶点，以限制具侵袭性的肠道细菌对黏膜的黏附、对炎症免疫反应的不当刺激以及随之而来的慢性肠道炎症的发展。
