The endogenous antimicrobial cathelicidin LL37 induces platelet activation and augments thrombus formation.

ABSTRACT: Platelet-associated complications including thrombosis, thrombocytopenia, and hemorrhage are commonly observed during various inflammatory diseases such as sepsis, inflammatory bowel disease, and psoriasis. Despite the reported evidence on numerous mechanisms/molecules that may contribute to the dysfunction of platelets, the primary mechanisms that underpin platelet-associated complications during inflammatory diseases are not fully established. Here, we report the discovery of formyl peptide receptor 2, FPR2/ALX, in platelets and its primary role in the development of platelet-associated complications via ligation with its ligand, LL37. LL37 acts as a powerful endogenous antimicrobial peptide, but it also regulates innate immune responses. We demonstrate the impact of LL37 in the modulati

SUBMITTER: Salamah MF 

PROVIDER: S-EPMC6234361 | biostudies-literature | 2018 Nov

REPOSITORIES: biostudies-literature