Toxoplasma gondii causes acute mucosal infections that are controlled by Ly6C+ inflammatory monocytes. In Nature Medicine, Grainger et al. show that Ly6C+ monocytes serve additional roles by suppressing collateral tissue damage that results from unstrained neutrophil activation. Ccr2−/− mice, which have defects in circulating Ly6C+ monocytes, have more severe gut pathology after infection with T. gondii. Commensal bacteria that escape into gut tissues elicit production of prostaglandin E2 (PGE2) by Ly6C+ monocytes. PGE2 inhibits the release of TNF and reactive oxygen from neutrophils in infected tissues. Inhibition of PGE2 production similarly exacerbates tissue pathology but does not alter monocyte control of T. gondii. Thus, exposure to gut bacteria induces protective properties of Ly6C+ monocytes to limit tissue damage during acute infection.

Nat. Med. (26 May 2013) doi:10.1038/nm.3189