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Cited by 264

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Inflammatory monocytes regulate pathologic responses to commensals during acute gastrointestinal infection

Open access
Grainger, John R, Wohlfert, Elizabeth A, Fuss, Ivan J, Bouladoux, Nicolas, Askenase, Michael H, Legrand, Fanny, Koo, Lily Y, Brenchley, Jason M, Fraser, Iain D C, Belkaid, Yasmine·2013·Nature Medicine

Abstract

The commensal flora can promote both immunity to pathogens and mucosal inflammation. How commensal-driven inflammation is regulated in the context of infection remains poorly understood. Here, we show that during acute mucosal infection of mice with Toxoplasma gondii, inflammatory monocytes acquire a tissue-specific regulatory phenotype associated with production of the lipid mediator prostaglandin E2 (PGE2). Notably, in response to commensals, inflammatory monocytes can directly inhibit neutrophil activation in a PGE2-dependent manner. Further, in the absence of inflammatory monocytes, mice develop severe neutrophil-mediated pathology in response to pathogen challenge that can be controlled by PGE2 analog treatment. Complementing these findings, inhibition of PGE2 led to enhanced neutrophil activation and host mortality after infection. These data demonstrate a previously unappreciated dual action of inflammatory monocytes in controlling pathogen expansion while limiting commensal-mediated damage to the gut. Collectively, our results place inflammatory monocyte–derived PGE2 at the center of a commensal-driven regulatory loop required to control host-commensal dialog during pathogen-induced inflammation.

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Crossref · 10.1038/nm.3189

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Metadata

Authors
Grainger, J. R., Wohlfert, E. A., Fuss, I. J., Bouladoux, N., Askenase, M. H., Legrand, F., Koo, L. Y., Brenchley, J. M., Fraser, I. D. C., & Belkaid, Y.
Venue
Nature Medicine
Published
2013-05-26
Volume
19
Issue
6
Pages
713-721
ISSN
  • 1078-8956 (ISSN-L)
  • 1546-170X
OpenAlex
W1992641640
Cited by
264
References
3
FWCI
11.33
Type
journal article
Language
en
Open access
green

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