Crth2 receptor signaling down-regulates lipopolysaccharide-induced NF-κB activation in murine macrophages via changes in intracellular calcium.

ABSTRACT: Prostaglandin D₂ and its cyclopentenone metabolites [cyclopentenone prostaglandins (CyPGs)], Δ¹²prostaglandin J₂ and 15-deoxy-Δ^12,14-prostaglandin J₂, act through 2 GPCRs, d-type prostanoid 1 and the chemoattractant receptor homologous molecule expressed on type 2 T-helper cells (Crth2). In addition to its role in allergy and asthma, the role of Crth2 in the resolution of inflammation, to mediate the proresolving functions of endogenous CyPGs, is not well understood. We investigated the regulation of LPS or zymosan-induced inflammatory response by signals from the Crth2 receptor in macrophages that lack Crth2 expression [knockout (KO)]. Increased expression of proinflammatory genes, including Tnf-α, was observed in Crth2 KO cell

SUBMITTER: Diwakar BT 

PROVIDER: S-EPMC6988853 | biostudies-literature | 2019 Nov

REPOSITORIES: biostudies-literature