生物膜
菌毛
免疫系统
微生物学
生物
细菌
炎症
寄主(生物学)
免疫
免疫学
大肠杆菌
生态学
遗传学
生物化学
基因
作者
Melissa Ellermann,Sartor Rb
出处
期刊:Journal of immunological sciences
[Sciaccess Publishers LLC]
日期:2018-03-01
卷期号:2 (2): 13-18
被引量:16
标识
DOI:10.29245/2578-3009/2018/2.1122
摘要
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.
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