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Cell Host Microbe. 2011 Nov 17;10(5):497-506. doi: 10.1016/j.chom.2011.10.006. Epub 2011 Oct 27.

Low-abundance biofilm species orchestrates inflammatory periodontal disease through the commensal microbiota and complement.

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  • 1Department of Microbiology and Immunology, University of Louisville School of Medicine, KY 40292, USA. g0haji01@louisville.edu

Abstract

Porphyromonas gingivalis is a low-abundance oral anaerobic bacterium implicated in periodontitis, a polymicrobial inflammatory disease, and the associated systemic conditions. However, the mechanism by which P. gingivalis contributes to inflammation and disease has remained elusive. Here we show that P. gingivalis, at very low colonization levels, triggers changes to the amount and composition of the oral commensal microbiota leading to inflammatory periodontal bone loss. The commensal microbiota and complement were both required for P. gingivalis-induced bone loss, as germ-free mice or conventionally raised C3a and C5a receptor-deficient mice did not develop bone loss after inoculation with P. gingivalis. These findings demonstrate that a single, low-abundance species can disrupt host-microbial homeostasis to cause inflammatory disease. The identification and targeting of similar low-abundance pathogens with community-wide impact may be important for treating inflammatory diseases of polymicrobial etiology.

Copyright © 2011 Elsevier Inc. All rights reserved.

PMID:
22036469
[PubMed - indexed for MEDLINE]
PMCID:
PMC3221781
Free PMC Article
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