Abstract Number: PB1833
Meeting: ISTH 2020 Congress
Background: Non-alcoholic fatty liver disease (NAFLD) is the main cause of chronic liver disease and ranges from simple steatosis to non-alcoholic steatohepatitis (NASH). Recently, a platelet role in NAFLD pathogenesis and progression has been reported in mouse models and in patients.
Aims: Aim of this study was to investigate the role of platelets in NAFLD as active players in liver disease and systemic inflammation.
Methods: We recruited 24 consecutive patients with biopsy-proven diagnosis of NAFLD. In these patients we investigated gene expression profile of the pro-inflammatory cytokines TLR2, TLR4, IL6, IL1R1, MPO, CXCR1, ICAM1,TNF and of hemostatic effectors GPVI, GPIB, F2R (Thrombin receptor PAR1), P2Y1, P2Y12 and thromboxane A2 receptor (TBXA2R) of circulating platelets. We measured plasma levels of leptin, IL-6, TNF-alpha, Il-8 and lipopolysaccharides (LPS) by ELISA commercial Kits. We measured platelet accumulation in liver sections using CD41 antibody, neutrophil extracellular traps (NET) deposition in liver sections using anti-H3 citrullinated histones antibodies.
Results: NAFLD patients had increased plasma levels of systemic inflammation markers and lipolysaccharides. We found an increased inflammatory gene expression in circulating platelets and not in leukocytes of NAFLD subjects compared with healthy controls. Expression of hemostatic genes was unchanged in NAFLD subjects compared with healthy controls. We demonstrated increased intrahepatic platelet accumulation that correlated with NAS score and intrahepatic neutrophil extracellular traps (NET) formation in liver biopsies of NAFLD patients. NET formation was higher in livers with higher NAS and inflammation scores.
Conclusions: The mutual relationship between liver platelet adhesion and NET formation, together with low-grade endotoxemia, low-grade systemic inflammation and pro-inflammatory changes of circulating platelets, suggests that platelets participate on systemic and liver inflammatory changes associated with NAFLD. Altogether, these results indicate that platelets may act primarily to protect the liver from invading microorganisms but contribute to the pathogenesis of liver damage and NAFLD progression.
To cite this abstract in AMA style:De Candia E, Miele L, Alberelli MA, Martini M, Landolfi R, Gasbarrini A, Grieco A. Platelets Are Active Players as Inflammatory Cells in Nonalcoholic Fatty Liver Disease [abstract]. Res Pract Thromb Haemost. 2020; 4 (Suppl 1). https://abstracts.isth.org/abstract/platelets-are-active-players-as-inflammatory-cells-in-nonalcoholic-fatty-liver-disease/. Accessed May 6, 2021.
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