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Treatment of platelets with riboflavin and ultraviolet light mediates complement activation and suppresses monocyte interleukin‐12 production in whole blood
Author(s) -
Loh Y. S.,
Dean M. M.,
Johnson L.,
Marks D. C.
Publication year - 2015
Publication title -
vox sanguinis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.68
H-Index - 83
eISSN - 1423-0410
pISSN - 0042-9007
DOI - 10.1111/vox.12283
Subject(s) - platelet , monocyte , lipopolysaccharide , whole blood , complement system , flow cytometry , cytokine , interleukin , immunology , chemistry , platelet activation , buffy coat , intracellular , microbiology and biotechnology , biology , biochemistry , immune system
Background and Objectives Pathogen inactivation ( PI ) and storage may alter the immunomodulatory capacity of platelets ( PLT s). The aim of this study was to examine the effect of PI (Riboflavin and ultraviolet light treatment) and storage on the capacity of PLT s to induce cytokine responses in recipient inflammatory cells. Materials and Methods A pool and split design was used to prepare untreated and PI ‐treated buffy coat‐derived platelet concentrates ( PC s). Samples were taken on days 2 and 7 postcollection and incubated with ABO /RhD‐matched fresh whole blood for 6 h with or without lipopolysaccharide ( LPS ). The intracellular production of IP ‐10, MCP ‐1, MIP ‐1α, IL ‐8, IL ‐6, IL ‐10, IL ‐12, TNF ‐α and MIP ‐1β in monocytes and neutrophils was assessed using flow cytometry. Complement proteins in PLT supernatants were measured using a cytometric bead array. Results PLT s and PLT supernatant (both untreated and PI ‐treated) resulted in modulation of intracellular MIP ‐1β and IL ‐12 production in monocytes. Compared to untreated PLT s, PI ‐treated PLT s resulted in significantly lower LPS ‐induced monocyte IL ‐12 production (day 7). The concentration of C3a and C5a (and their desArg forms) was significantly increased in PLT supernatants following PI . Conclusion PI results in decreased LPS ‐induced monocyte IL ‐12 production and increased complement activation. The association between platelet‐induced complement activation and IL ‐12 production warrants further investigation.