A microbial symbiosis factor prevents intestinal inflammatory disease

Sarkis K. Mazmanian (), June L. Round and Dennis L. Kasper ()
Additional contact information
Sarkis K. Mazmanian: California Institute of Technology, Pasadena, California 91125, USA
June L. Round: California Institute of Technology, Pasadena, California 91125, USA
Dennis L. Kasper: Channing Laboratory, Brigham & Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA

Nature, 2008, vol. 453, issue 7195, 620-625

Abstract: Abstract Humans are colonized by multitudes of commensal organisms representing members of five of the six kingdoms of life; however, our gastrointestinal tract provides residence to both beneficial and potentially pathogenic microorganisms. Imbalances in the composition of the bacterial microbiota, known as dysbiosis, are postulated to be a major factor in human disorders such as inflammatory bowel disease. We report here that the prominent human symbiont Bacteroides fragilis protects animals from experimental colitis induced by Helicobacter hepaticus, a commensal bacterium with pathogenic potential. This beneficial activity requires a single microbial molecule (polysaccharide A, PSA). In animals harbouring B. fragilis not expressing PSA, H. hepaticus colonization leads to disease and pro-inflammatory cytokine production in colonic tissues. Purified PSA administered to animals is required to suppress pro-inflammatory interleukin-17 production by intestinal immune cells and also inhibits in vitro reactions in cell cultures. Furthermore, PSA protects from inflammatory disease through a functional requirement for interleukin-10-producing CD4+ T cells. These results show that molecules of the bacterial microbiota can mediate the critical balance between health and disease. Harnessing the immunomodulatory capacity of symbiosis factors such as PSA might potentially provide therapeutics for human inflammatory disorders on the basis of entirely novel biological principles.

Date: 2008
References: Add references at CitEc
Citations: View citations in EconPapers (11)

Downloads: (external link)
https://www.nature.com/articles/nature07008 Abstract (text/html)
Access to the full text of the articles in this series is restricted.

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:453:y:2008:i:7195:d:10.1038_nature07008

Ordering information: This journal article can be ordered from
https://www.nature.com/

DOI: 10.1038/nature07008

Access Statistics for this article

Nature is currently edited by Magdalena Skipper

More articles in Nature from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().