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The artificial surface‐induced whole blood inflammatory reaction revealed by increases in a series of chemokines and growth factors is largely complement dependent
Author(s) -
Lappegård K. T.,
Bergseth G.,
Riesenfeld J.,
Pharo A.,
Magotti P.,
Lambris J. D.,
Mollnes T. E.
Publication year - 2008
Publication title -
journal of biomedical materials research part a
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.849
H-Index - 150
eISSN - 1552-4965
pISSN - 1549-3296
DOI - 10.1002/jbm.a.31750
Subject(s) - proinflammatory cytokine , chemokine , complement system , inflammation , cytokine , immunology , materials science , pharmacology , medicine , immune system
Exposing blood to an artificial surface results in a systemic inflammatory response, including cytokine release and complement activation. We studied the artificial surface‐induced inflammation in human whole blood using an extensive panel of inflammatory mediators including proinflammatory cytokines, chemokines and growth‐factors and investigated the role of the complement system in the induction of this response. Using multiplex technology, 27 different inflammatory mediators were measured after circulating blood for 4 hours in polyvinyl chloride tubing. The C3 inhibitor compstatin was used to block complement activation. A significant ( p < 0.05) increase in 14 of the 27 mediators was induced by the surface, of which 7 were chemokines (IL‐8, MCP‐1, MIP‐1α, MIP‐1β, RANTES, eotaxin and IP‐10) and 5 were growth‐factors (G‐CSF, GM‐CSF, VEGF, PDGF and FGF). The traditional proinflammatory cytokines like IL‐1β, TNFα and IL‐6 were not induced, although IL‐6, as well as IL‐15 and IL‐17 increased if the surface was coated with highly bioincompatible laminaran. Inhibition of complement activation with compstatin significantly ( p < 0.05) reduced the formation of 12 of the 14 mediators. For 10 of the 12 mediators, the inhibition was by 2/3 or more, for the remaining two the inhibition was more moderate. A highly biocompatible heparin‐coated PVC surface was used as negative control and completely abolished the whole inflammatory response. The artificial surface PVC markedly induced a broad spectrum of chemokines and growth‐factors, which was largely dependent on activation of complement. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res, 2008