Pro-inflammatory effects after platelet transfusion: a review.

BACKGROUND AND OBJECTIVES: Platelet has been linked to thrombosis in several studies. Inflammation is closely intertwined with thrombosis and occurs consecutively; it is therefore conceivable that platelet transfusions perform an increasingly vital role in inflammation. As platelet transfusions have been a significant therapeutic approach in patients for decades, serious risks including viral transmission, bacterial sepsis and acute lung injury have been demonstrated by retrospective studies and randomized clinical trials. Recent data suggest associations among platelet transfusion and pro-inflammatory responses. MATERIALS AND METHODS: A systematic review (from 2014 to 2019) on English literatures was conducted. Data on platelet transfusion-related reactions were abstracted. Preset inclusion and exclusion criteria were applied to identify all eligible articles. RESULTS: All patients abstracted have received platelet transfusion. This new review focuses on recent 5-year advances (from 2014 to 2019) to have found that the platelet transfusion as pro-inflammatory process, concerning secretion of platelet microparticles and other inflammatory factors. CONCLUSION: It can be hypothesized that the platelet microparticles or biological response modifier pathways might be innovative and therapeutic approaches to improving platelet transfusion and pretransfusion manipulations to reduce transfusion-related adverse reactions and therefore improve the efficacy and safety of this wide-employed therapy.

Ethanol exposure leads to disorder of blood island formation in early chick embryo.

Ethanol's effect on embryonic vasculogenesis and its underlying mechanism is obscure. Using VE-cadherin in situ hybridization, we found blood islands formation was inhibited in area opaca, but abnormal VE-cadherin+ cells were seen in area pellucida. We hypothesise ethanol may affect blood island progenitor cell migration and differentiation. DiI and in vitro experiments revealed ethanol inhibited cell migration, Quantitative PCR analysis revealed that ethanol exposure enhanced cell differentiation in area pellucida of HH5 chick embryos and repressed cell differentiation in area pellucida of HH8 chick embryos. By exposing to 2,2'-azobis-amidinopropane dihydrochloride, a ROS inducer, which gave a similar anti-vasculogenesis effect as ethanol and this anti-vasculogenesis effect could be reversed by vitamin C. Overall, exposing early chick embryos to ethanol represses blood island progenitor cell migration but disturbed differentiation at a different stage, so that the disorder of blood island formation occurs through excess ROS production and altered vascular-associated gene expression.