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Immunity. 2008 Aug 15;29(2):306-17. doi: 10.1016/j.immuni.2008.05.019.

Gr1(+) inflammatory monocytes are required for mucosal resistance to the pathogen Toxoplasma gondii.

Author information

1
Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, MO 63110, USA.

Erratum in

  • Immunity. 2008 Oct;29(4):660.

Abstract

The enteric pathogen Toxoplasma gondii is controlled by a vigorous innate T helper 1 (Th1) cell response in the murine model. We demonstrated that after oral infection, the parasite rapidly recruited inflammatory monocytes [Gr1(+) (Ly6C(+), Ly6G(-)) F4/80(+)CD11b(+)CD11c(-)], which established a vital defensive perimeter within the villi of the ileum in the small intestine. Mice deficient of the chemokine receptor CCR2 or the ligand CCL2 failed to recruit Gr1(+) inflammatory monocytes, whereas dendritic cells and resident tissue macrophages remained unaltered. The selective lack of Gr1(+) inflammatory monocytes resulted in an inability of mice to control replication of the parasite, high influx of neutrophils, extensive intestinal necrosis, and rapid death. Adoptive transfer of sorted Gr1(+) inflammatory monocytes demonstrated their ability to home to the ileum in infected animals and protect Ccr2(-/-) mice, which were otherwise highly susceptible to oral toxoplasmosis. Collectively, these findings illustrate the critical importance of inflammatory monocytes as a first line of defense in controlling intestinal pathogens.

PMID:
18691912
PMCID:
PMC2605393
DOI:
10.1016/j.immuni.2008.05.019
[Indexed for MEDLINE]
Free PMC Article

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