GPR35 mediates monocyte recruitment to the sites of Listeria monocytogenes infection

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Recruitment of Ly6C hi monocytes to infection sites critically contributes to the clearance of microbial pathogens. However, the mechanism regulating their migration from the peripheral blood to the infected sites remains unresolved. In this study, we demonstrate that G protein-coupled receptor GPR35 is required for the entry of circulating Ly6C hi monocytes into the sites of Listeria monocytogenes infection. Gpr35 -/- mice showed a decrease in Ly6C hi monocyte recruitment to the cecum and colon after oral administration of L. monocytogenes. They also exhibited a reduction in Ly6C hi monocytes in the liver and spleen upon intravenous infection. Mechanistically, GPR35 signaling enhanced Mac-1- and LFA-1-dependent Ly6C hi monocyte adhesion to ICAM-1, and GPR35-dependent integrin activation was important for their in vivo recruitment to infected sites. A potential GPR35-reactive metabolite, lysophosphatidic acid, accumulated around the bacterial foci near to the blood vessels. In addition, the GPR35 signal induced TNF-α production by Ly6C hi Sca-1 + monocytes and restricted the bacterial burden of L. monocytogenes. Collectively, GPR35-mediated signaling provides the molecular cue for elimination of L. monocytogenes by recruiting circulating Ly6C hi monocytes to the infected sites where they produce TNF-α.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.