Format

Send to

Choose Destination
See comment in PubMed Commons below
Cell Host Microbe. 2015 May 13;17(5):672-80. doi: 10.1016/j.chom.2015.04.002.

Colitogenic Bacteroides thetaiotaomicron Antigens Access Host Immune Cells in a Sulfatase-Dependent Manner via Outer Membrane Vesicles.

Author information

1
Department of Pathology and Immunology, Washington University School of Medicine, 660 S. Euclid Avenue, St. Louis, MO 63110, USA; Department of Pediatrics, Washington University School of Medicine, 660 S. Euclid Avenue, St. Louis, MO 63110, USA.
2
Department of Pathology and Immunology, Washington University School of Medicine, 660 S. Euclid Avenue, St. Louis, MO 63110, USA.
3
Department of Microbiology and Immunology, University of Michigan Medical School, 1500 E. Medical Center Drive, Ann Arbor, MI 48109, USA.
4
Department of Medical Biochemistry, University of Gothenburg, Box 440, 405 30 Gothenburg, Sweden.
5
Department of Pathology and Immunology, Washington University School of Medicine, 660 S. Euclid Avenue, St. Louis, MO 63110, USA. Electronic address: allen@pathology.wustl.edu.
6
Department of Microbiology and Immunology, University of Michigan Medical School, 1500 E. Medical Center Drive, Ann Arbor, MI 48109, USA. Electronic address: emartens@umich.edu.
7
Department of Pathology and Immunology, Washington University School of Medicine, 660 S. Euclid Avenue, St. Louis, MO 63110, USA. Electronic address: stappenb@pathology.wustl.edu.

Abstract

Microbes interact with the host immune system via several potential mechanisms. One essential step for each mechanism is the method by which intestinal microbes or their antigens access specific host immune cells. Using genetically susceptible mice (dnKO) that develop spontaneous, fulminant colitis, triggered by Bacteroides thetaiotaomicron (B. theta), we investigated the mechanism of intestinal microbial access under conditions that stimulate colonic inflammation. B. theta antigens localized to host immune cells through outer membrane vesicles (OMVs) that harbor bacterial sulfatase activity. We deleted the anaerobic sulfatase maturating enzyme (anSME) from B. theta, which is required for post-translational activation of all B. theta sulfatase enzymes. This bacterial mutant strain did not stimulate colitis in dnKO mice. Lastly, access of B. theta OMVs to host immune cells was sulfatase dependent. These data demonstrate that bacterial OMVs and associated enzymes promote inflammatory immune stimulation in genetically susceptible hosts.

PMID:
25974305
PMCID:
PMC4432250
DOI:
10.1016/j.chom.2015.04.002
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Support Center