July 28, 2014

Regulation of the gut microbiota by the mucosal immune system in mice

  1. Naohiro Inohara
+Author Affiliations
  1. Department of Pathology, University of Michigan Medical School, 1150W. Medical Center Drive, Ann Arbor, MI 48109, USA
  1. Correspondence to: N. Inohara; E-mail: ino@umich.edu
  • Received April 7, 2014.
  • Accepted April 28, 2014.

Abstract

The benefits of commensal bacteria to the health of the host have been well documented, such as providing stimulation to potentiate host immune responses, generation of useful metabolites, and direct competition with pathogens. However, the ability of the host immune system to control the microbiota remains less well understood. Recent microbiota analyses in mouse models have revealed detailed structures and diversities of microbiota at different sites of the digestive tract in mouse populations. The contradictory findings of previous studies on the role of host immune responses in overall microbiota composition are likely attributable to the high β-diversity in mouse populations as well as technical limitations of the methods to analyze microbiota. The host employs multiple systems to strictly regulate their interactions with the microbiota. A spatial segregation between the host and microbiota is achieved with the mucosal epithelium, which is further fortified with a mucus layer on the luminal side and Paneth cells that produce antimicrobial peptides. When commensal bacteria or pathogens breach the epithelial barrier and translocate to peripheral tissues, the host immune system is activated to eliminate them. Defective segregation and tissue elimination of commensals result in exaggerated inflammatory responses and possibly death of the host. In this review, we discuss the current understanding of mouse microbiota, its common features with human microbiota, the technologies utilized to analyze microbiota, and finally the challenges faced to delineate the role of host immune responses in the composition of the luminal microbiota.

This Article

  1. Int. Immunol.doi: 10.1093/intimm/dxu049
  1. All Versions of this Article:
    1. dxu049v1
    2. dxu049v2 most recent
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