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Sci Rep. 2017 Dec 18;7(1):17707. doi: 10.1038/s41598-017-18014-5.

A gut pathobiont synergizes with the microbiota to instigate inflammatory disease marked by immunoreactivity against other symbionts but not itself.

Author information

1
Department of Food Science and Technology, University of Nebraska-Lincoln, Lincoln, Nebraska, USA.
2
Department of Statistics, University of Nebraska-Lincoln, Lincoln, Nebraska, USA.
3
Department of Veterinary Pathology, College of Veterinary Medicine, Iowa State University, Ames, Iowa, USA.
4
Department of Agricultural, Food and Nutritional Science, University of Alberta, Edmonton, Alberta, Canada.
5
Department of Biological Sciences -Lincoln, University of Alberta, Edmonton, Alberta, Canada.
6
Department of Food Science and Technology, University of Nebraska-Lincoln, Lincoln, Nebraska, USA. aramer-tait2@unl.edu.

Abstract

Inflammatory bowel diseases (IBD) are likely driven by aberrant immune responses directed against the resident microbiota. Although IBD is commonly associated with a dysbiotic microbiota enriched in putative pathobionts, the etiological agents of IBD remain unknown. Using a pathobiont-induced intestinal inflammation model and a defined bacterial community, we provide new insights into the immune-microbiota interactions during disease. In this model system, the pathobiont Helicobacter bilis instigates disease following sub-pathological dextran sulfate sodium treatment. We show that H. bilis causes mild inflammation in mono-associated mice, but severe disease in the presence of a microbiota, demonstrating synergy between the pathobiont and microbiota in exacerbating pathology. Remarkably, inflammation depends on the presence of H. bilis, but is marked by a predominant Th17 response against specific members of the microbiota and not the pathobiont, even upon the removal of the most immune-dominant taxa. Neither increases in pathobiont burden nor unique changes in immune-targeted microbiota member abundances are observed during disease. Collectively, our findings demonstrate that a pathobiont instigates inflammation without being the primary target of a Th17 response or by altering the microbiota community structure. Moreover, our findings point toward monitoring pathobiont-induced changes in microbiota immune targeting as a new concept in IBD diagnotics.

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