Abstract

UV light can be used to irradiate platelets to reduce immune responses and activate chemically-mediated pathogen reduction agents. Platelets subjected to UV-based processing methods develop demonstrable losses of in vivo performance. We compared the “lesions” induced by the different wavelengths of UV light on human platelet performance in a SCID mouse animal model of recovery and survival. Previously we demonstrated that severe combined immunodeficient (SCID) mice could be used as an animal model to identify both severely damaged (Blood 106(11), p537a, 2005) and moderately damaged human platelets (Blood 108(11), p175–176a, 2006). Apheresis human platelets, stored for 1 or 7 days, were exposed to UVA(320–400 nm) or UVB(290–320 nm) light for 20 min (4.8 J/mL) or 40 min (9.6 J/mL). Control platelets were processed in the same manner without UV exposure. Effects on platelets were compared on platelet counts, activation measured by p-selectin (anti-human CD62P, clone AK-4) and in vivo recovery. Platelet counts and in vivo recovery are expressed as % of control platelets, p-selectin measurement represents % of cells expressing the antigen. For in vivo recovery, approximately 1×10 9 platelets (UV-treated or control) were injected into the tail vein of SCID mice (n=4 per each condition) and serial blood samples were collected. Human platelets were detected in mouse whole blood by flow cytometry using an anti-human GPIIbIIIa mAb (clone P2). Recovery was defined as percent of human platelets in mouse circulation 30 minutes post infusion. Comparison of recovery between control and UV treatment platelets was done at 2 hours post infusion as shown in Table 1.

These results indicate that UVA produces less activation of platelets and less damage to human platelets recognized by the in vivo model than UVB. The UVA lesion detected by increased in vivo clearance is not cumulative in that longer exposures do not cause an increased loss of in vivo recovery. In comparison, UVB mediated damage is associated with lower in vivo recovery and the damage appears to be cumulative with longer exposure. These differences suggest that UVA and UVB exposure may produce platelet lesions through different mechanism(s). Further investigation into the molecular mechanisms of UVA and UVB lesions may lead to methods that could reduce the negative aspects of UV exposure. The findings and conclusions in this abstract have not been formally disseminated by the Food and Drug Administration and should not be construed to represent any Agency determination or policy.

Table 1
TreatmentDay 1Day 7
1= percent of control platelets;2=human platelet recovery in SCID mouse model 
  Platelet count1 P-selectin (%) In vivo recovery2 Platelet count1 P-selectin (%) In vivo recovery2 
UVA 20 min 100 13.3±2.7 55.2±7.6 100 20.3±3.8 58.2±4.9 
 40 min 100 9.9±0.9 55.5±2.9 100 17.3±2.9 54.3±6.7 
UVB 20 min 82±3.7 34.6±5.0 30.8±8.9 86±5.3 51.1±6.4 18.5±4.6 
 40 min 51±10.1 29.5±1.5 6.9±2.6 63±10.5 36.2±1.8 2.47±0.9 
TreatmentDay 1Day 7
1= percent of control platelets;2=human platelet recovery in SCID mouse model 
  Platelet count1 P-selectin (%) In vivo recovery2 Platelet count1 P-selectin (%) In vivo recovery2 
UVA 20 min 100 13.3±2.7 55.2±7.6 100 20.3±3.8 58.2±4.9 
 40 min 100 9.9±0.9 55.5±2.9 100 17.3±2.9 54.3±6.7 
UVB 20 min 82±3.7 34.6±5.0 30.8±8.9 86±5.3 51.1±6.4 18.5±4.6 
 40 min 51±10.1 29.5±1.5 6.9±2.6 63±10.5 36.2±1.8 2.47±0.9 

Author notes

Disclosure: No relevant conflicts of interest to declare.