The intestinal microbiota contributes to the ability of helminths to modulate allergic inflammation.

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State: Public
Version: Final published version
License: CC BY-NC-ND 4.0
Serval ID
serval:BIB_7177571B08CD
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
The intestinal microbiota contributes to the ability of helminths to modulate allergic inflammation.
Journal
Immunity
Author(s)
Zaiss M.M., Rapin A., Lebon L., Dubey L.K., Mosconi I., Sarter K., Piersigilli A., Menin L., Walker A.W., Rougemont J., Paerewijck O., Geldhof P., McCoy K.D., Macpherson A.J., Croese J., Giacomin P.R., Loukas A., Junt T., Marsland B.J., Harris N.L.
ISSN
1097-4180 (Electronic)
ISSN-L
1074-7613
Publication state
Published
Issued date
17/11/2015
Peer-reviewed
Oui
Volume
43
Number
5
Pages
998-1010
Language
english
Notes
Publication types: Journal ArticlePublication Status: ppublish
Abstract
Intestinal helminths are potent regulators of their host's immune system and can ameliorate inflammatory diseases such as allergic asthma. In the present study we have assessed whether this anti-inflammatory activity was purely intrinsic to helminths, or whether it also involved crosstalk with the local microbiota. We report that chronic infection with the murine helminth Heligmosomoides polygyrus bakeri (Hpb) altered the intestinal habitat, allowing increased short chain fatty acid (SCFA) production. Transfer of the Hpb-modified microbiota alone was sufficient to mediate protection against allergic asthma. The helminth-induced anti-inflammatory cytokine secretion and regulatory T cell suppressor activity that mediated the protection required the G protein-coupled receptor (GPR)-41. A similar alteration in the metabolic potential of intestinal bacterial communities was observed with diverse parasitic and host species, suggesting that this represents an evolutionary conserved mechanism of host-microbe-helminth interactions.
Pubmed
Web of science
Open Access
Yes
Create date
11/01/2016 17:51
Last modification date
01/02/2024 7:11
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