The Non-Hemostatic Aspects of Transfused Platelets

Abstract

Platelets transfusion is a safe process, but during or after the process, the recipient may experience an adverse reaction and occasionally a serious adverse reaction (SAR). In this review, we focus on the inflammatory potential of platelet components (PCs) and their involvement in SARs. Recent evidence has highlighted a central role for platelets in the host inflammatory and immune responses. Blood platelets are involved in inflammation and various other aspects of innate immunity through the release of a plethora of immunomodulatory cytokines, chemokines, and associated molecules, collectively termed biological response modifiers that behave like ligands for endothelial and leukocyte receptors and for platelets themselves. The involvement of PCs in SARs—particularly on a critically ill patient’s context—could be related, at least in part, to the inflammatory functions of platelets, acquired during storage lesions. Moreover, we focus on causal link between platelet activation and immune-mediated disorders (transfusion-associated immunomodulation, platelets, polyanions, and bacterial defense and alloimmunization). This is linked to the platelets’ propensity to be activated even in the absence of deliberate stimuli and to the occurrence of time-dependent storage lesions.

Pathogen inactivation with amotosalen plus UVA illumination minimally impacts microRNA expression in platelets during storage under standard blood banking conditions

“…Down regulation of miR‐96‐5p in PI‐PAS compared to C‐PAS might be related to accelerated granule release in the PI‐PAS as demonstrated by increased concentration of PF‐4, sP‐selectin, and CD40L especially on Day 4. All these factors are released by platelet α‐granules . The release of platelet factors from there granules is under the control of v‐SNEARE complex containing endobrevin/Vamp8 .…”

Inhibition of the CD40/CD40L complex protects mice against ALI‐induced pancreas degradation

“…CD40L is a primarily a platelet‐derived proinflammatory mediator found in cell‐associated and soluble forms. Our group and others described it to be present in platelet concentrates, where it accumulates during storage . CD40L binds monocytes, macrophages, and neutrophils.…”

“…Remarkably, Patel et al described, in a swine model, that RBC transfusion in the absence of cardiopulmonary bypass, also resulted in renal injury, characterized by endothelial injury, microvascular endothelial dysfunction, platelet activation, and equivalent cortical tubular epithelial phenotypic changes. Platelets transfusion has been associated with vascular inflammatory and immune complications similar to RBC transfusion …”

“…[30][31][32] Remarkably, Patel et al 33,34 described, in a swine model, that RBC transfusion in the absence of cardiopulmonary bypass, also resulted in renal injury, characterized by endothelial injury, microvascular endothelial dysfunction, platelet activation, and equivalent cortical tubular epithelial phenotypic changes. Platelets transfusion has been associated with vascular inflammatory and immune complications [35][36][37] similar to RBC transfusion. 38,39 Histologic evaluation of pancreatic lesions and the measurement of plasma-soluble markers, reflecting degradation of the tissue, suggested that multiple organ injury occurred in this murine model of ALI.…”

“…Our group and others described it to be present in platelet concentrates, where it accumulates during storage. 37,[73][74][75][76][77] CD40L binds monocytes, macrophages, and neutrophils. Khan et al 78 revealed that CD40L primes neutrophils through CD40 and identified CD40L as a possible cofactor in TRALI because its concentration in transfused platelet concentrates having been associated with TRALI cases was significantly higher than in the control units.…”