To the top

Page Manager: Webmaster
Last update: 9/11/2012 3:13 PM

Tell a friend about this page
Print version

Colitogenic Bacteroides t… - University of Gothenburg, Sweden Till startsida
Sitemap
To content Read more about how we use cookies on gu.se

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

Journal article
Authors C. A. Hickey
K. A. Kuhn
D. L. Donermeyer
N. T. Porter
Chunsheng S. Jin
E. A. Cameron
H. Jung
G. E. Kaiko
M. Wegorzewska
N. P. Malvin
R. W. P. Glowacki
Gunnar C. Hansson
P. M. Allen
E. C. Martens
T. S. Stappenbeck
Published in Cell Host & Microbe
Volume 17
Issue 5
Pages 672-680
ISSN 1931-3128
Publication year 2015
Published at Institute of Biomedicine
Pages 672-680
Language en
Links dx.doi.org/10.1016/j.chom.2015.04.0...
Keywords INFLAMMATORY-BOWEL-DISEASE, HUMAN GUT SYMBIONT, MUC2 MUCIN, BACTERIAL, SYMBIONT, SMALL-INTESTINE, COMMENSAL, COLON, MACROPHAGES, COLITIS, PURIFICATION, Microbiology, Parasitology, Virology
Subject categories Microbiology in the medical area

Abstract

Microbes interact with the host immune system via several potential mechanisms. One essential step for each mechanismis themethod 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 inflammatoryimmune stimulation in genetically susceptible hosts.

Page Manager: Webmaster|Last update: 9/11/2012
Share:

The University of Gothenburg uses cookies to provide you with the best possible user experience. By continuing on this website, you approve of our use of cookies.  What are cookies?