Faber Franziska, Bäumler Andreas J
Department of Medical Microbiology and Immunology, School of Medicine, University of California at Davis, One Shields Avenue, Davis, CA 95616, USA.
Department of Medical Microbiology and Immunology, School of Medicine, University of California at Davis, One Shields Avenue, Davis, CA 95616, USA.
Immunol Lett. 2014 Dec;162(2 Pt A):48-53. doi: 10.1016/j.imlet.2014.04.014. Epub 2014 May 4.
The intestinal epithelium is a single cell barrier separating a sterile mucosal tissue from a large microbial community dominated by obligate anaerobic bacteria, which inhabit the gut lumen. To maintain mucosal integrity, any breach in the epithelial barrier needs to be met with an inflammatory host response designed to repel microbial intruders from the tissue, protect the mucosal surface and repair injuries to the epithelium. In addition, inflammation induces mechanisms of nutritional immunity, which limit the availability of metals in the intestinal lumen, thereby imposing new selective forces on microbial growth. However, the inflammatory host response also has important side effects. A by-product of producing reactive oxygen and nitrogen species aimed at eradicating microbial intruders is the luminal generation of exogenous electron acceptors. The presence of these electron acceptors creates a new metabolic niche that is filled by facultative anaerobic bacteria. Here we review the changes in microbial nutrient utilization that accompany intestinal inflammation and the consequent changes in the composition of gut-associated microbial communities.
肠道上皮是一道单细胞屏障,将无菌的黏膜组织与以专性厌氧菌为主导的庞大微生物群落分隔开来,这些厌氧菌栖息于肠腔。为维持黏膜完整性,上皮屏障的任何破损都需要引发宿主炎症反应,旨在将微生物入侵者从组织中击退、保护黏膜表面并修复上皮损伤。此外,炎症会诱导营养免疫机制,限制肠腔内金属的可用性,从而对微生物生长施加新的选择压力。然而,宿主炎症反应也有重要的副作用。旨在根除微生物入侵者而产生的活性氧和氮物种的一个副产品是肠腔内产生外源性电子受体。这些电子受体的存在创造了一个新的代谢生态位,由兼性厌氧菌占据。在此,我们综述了伴随肠道炎症的微生物营养利用变化以及肠道相关微生物群落组成随之发生的变化。