Ultraviolet C light pathogen inactivation treatment of platelet concentrates preserves integrin activation but affects thrombus formation kinetics on collagen in vitro

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Ultraviolet (UV) light illumination in the presence of exogenously added photosensitizers has been used to inactivate pathogens in platelet (PLT) concentrates for some time. The THERAFLEX UV-C system, however, illuminates PLT concentrates with UV-C light without additional photoactive compounds. In this study residual PLT function is measured in a comprehensive paired analysis of UV-C–treated, gamma-irradiated, and untreated control PLT concentrates.


STUDY DESIGN AND METHODS: A pool-and-split design was used with buffy coat–derived PLT concentrates in 65% SSP+ additive solution. Thrombus formation kinetics in microfluidic flow chambers onto immobilized collagen was investigated with real-time video microscopy. PLT aggregation, membrane markers, and cellular metabolism were determined concurrently.


Compared to gamma-treated and untreated controls, UV-C treatment significantly affected thrombus formation rates on Days 5 and 7, not Day 2. PLT degranulation (P-selectin) and PLT apoptosis (annexin V binding) was slightly but significantly increased from Day 2 on. UV-C treatment moreover induced integrin αIIbβ3 conformational changes reminiscent of activation. However, subsequent integrin activation by either PAR1-activating hexapeptide (PAR1AP) or convulxin was unaffected. This was confirmed by PLT aggregation studies induced with collagen, PAR1AP, and ristocetin at two different agonist concentrations. Finally, UV-C slightly increased lactic acid production rates, resulting in significantly decreased pH on Days 5 and 7, but never dropped below 7.2.


UV-C pathogen inactivation treatment slightly but significantly increases PLT activation markers but does not profoundly influence activatability nor aggregation. The treatment does, however, attenuate thrombus formation kinetics in vitro in microfluidic flow chambers, especially after storage.

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