Monocyte upregulation of podoplanin during early sepsis induces complement inhibitor release to protect liver function.

ABSTRACT: Multiple organ failure in sepsis is a progressive failure of several interdependent organ systems. Liver dysfunction occurs early during sepsis and is directly associated with patient death; however, the underlying mechanism of liver dysfunction is unclear. Platelet transfusion benefits patients with sepsis, and inhibition of complement activation protects liver function in septic animals. Herein, we explored the potential link between platelets, complement activation, and liver dysfunction in sepsis. We found that deletion of platelet C-type lectin-like receptor 2 (CLEC-2) exacerbated liver dysfunction in early sepsis. Platelet CLEC-2-deficient mice exhibited higher complement activation, more severe complement attack in the liver, and lower plasma levels of complement inhibitors at early

SUBMITTER: Xie Z 

PROVIDER: S-EPMC7406268 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature