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In Situ Deposition of Complement in Human Acute Brain Ischaemia
Author(s) -
Pedersen E. D.,
Løberg E. M.,
Vege E.,
Daha M. R.,
Mæhlen J.,
Mollnes T. E.
Publication year - 2009
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.2009.02253.x
Subject(s) - complement system , ischemia , ischaemic stroke , immunohistochemistry , pathology , complement (music) , cd59 , human brain , complement membrane attack complex , serine protease , alternative complement pathway , biology , complement factor b , complement c1q , immunology , medicine , immune system , protease , neuroscience , biochemistry , enzyme , gene , phenotype , complementation
Experimental animal models indicate that complement contributes to tissue damage during brain ischaemia and stroke, but limited data are available for a role of the complement in human stroke. We, therefore, evaluated whether acute ischaemia leads to complement activation in human brain. Indirect immunohistochemical staining was performed on paraffin‐embedded, formalin‐fixed human brain from 10 patients and 10 controls. Complement components C1q, C3c and C4d were detected in all ischaemic lesions, suggesting activation via the classical pathway. C9, C‐reactive protein and IgM were detected in necrotic zones. Marked CD59 and weak CD55 expression were found in normal brains, but these complement regulators were virtually absent in ischaemic lesions. Modest amounts of mannose‐binding lectin (MBL), MBL‐associated serine protease‐2 and factor B were found in both ischaemic lesions and controls. These data suggest that increased deposition of complement components combined with decreased expression of complement regulators is a possible mechanism of tissue damage during ischaemia in human brain.