Systemic complement activation following human acute ischaemic stroke

SUMMARY The brain tissue damage after stroke is mediated partly by inflammation induced by ischaemia–reperfusion injury where the complement system plays a pivotal role. In the present study we investigated systemic complement activation and its relation to C‐reactive protein (CRP), a known complement activator, and other inflammatory mediators after acute ischaemic stroke. Sequential plasma samples from 11 acute stroke patients were obtained from the time of admittance to hospital and for a follow‐up period of 12 months. Nine healthy gender‐ and age‐matched subjects served as controls. The terminal SC5b‐9 complement complex (TCC), CRP, soluble adhesion molecules (L‐, E‐ and P‐ selectin, ICAM, VCAM) and cytokines [tumour necrosis factor (TNF)‐ α , interleukin (IL)‐1 β , IL‐8] were analysed. All parameters were within normal values and similar to the controls the first hours after stroke. Terminal complement complex (TCC) increased significantly from 0·54 to 0·74 AU/ml at 72 h ( P  = 0·032), reached maximum at 7 days (0·90 AU/ml, P  < 0·001), was still significantly increased at 12 days (0·70 AU/ml, P  = 0·009) and thereafter normalized. CRP increased significantly from 1·02 to 2·11 mg/l at 24 h ( P  = 0·023), remained significantly increased for 1 week (2·53–2·94 mg/l, P  = 0·012–0·017) and thereafter normalized. TCC and C‐reactive protein (CRP) correlated significantly ( r  = 0·36, P  < 0·001). The increase in TCC and CRP correlated to the size of infarction ( r  = 0·80 and P  = 0·017 for TCC; r  = 0·72 and P  = 0·043 for CRP). No significant changes were seen for adhesion molecules and cytokines. In conclusion, transitory systemic complement activation takes place after stroke. The early rise in CRP and the following TCC increase suggest a possible role for CRP in complement activation, which may contribute to inflammation after stroke.