Impact of platelet transfusions on plasma proteomes in controlled endotoxemia and in hemato-oncological patients.

Background: Inflammation is a hallmark of patients that receive platelet transfusions, including critically ill and hemato-oncological patients. Platelet transfusions have been suggested to exacerbate inflammatory conditions, resulting in transfusion-related complications. Here, we used plasma proteomics to study the impact of platelet transfusions under inflammatory conditions.

Methods: Plasma proteomics was performed in samples from two studies: (1) 252 samples from healthy volunteers from 36 cases divided into groups (n = 6) with and without controlled endotoxemia, each with different platelet products, and (2) 54 samples from 27 transfusion events in hemato-oncological patients (n = 14). Both studies had samples pre- and post-transfusions.

Results: Controlled endotoxemia elicited a shared inflammatory response across all healthy volunteers. This response was characterized by increased abundance of two kinetically distinct protein clusters, an initial cluster associated with degranulation and inflammation (i.e., S100A9 and MMP9) followed by a cluster of acute-phase proteins (i.e., SAA and CRP). Autologous platelet transfusions in healthy individuals did not induce transfusion-specific changes in plasma protein levels, nor did they exacerbate the effect of controlled endotoxemia. In hemato-oncological patients, we found a transfusion-specific response restricted to alterations in platelet basic protein (PPBP) levels. No additional changes in plasma protein profiles associated with inflammation or dysregulated processes were observed following platelet transfusions.

Discussion: Platelet transfusions did not induce specific quantitative changes in plasma protein levels in healthy volunteers. Nonetheless, they were associated with increased levels of PPBP in hemato-oncological patients. In general, no evidence of inflammation or other dysregulated processes was observed following platelet transfusions.