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Complement Cascade Activation After an Acute Psychological Stress Task

From the School of Sport and Exercise Sciences (V.E.B., K.M.E., C.R., D.C.) and the Department of Immunology (M.D.), University of Birmingham, Birmingham, UK.

Address correspondence and reprint requests to Victoria Burns, School of Sport and Exercise Sciences, University of Birmingham, Birmingham, B15 2TT, UK. E-mail: V.E.Burns{at}bham.ac.uk

Objective: To examine complement cascade activation after an acute psychological stress task. Psychological stress has been implicated in the exacerbation of inflammatory disorders. Although the complement cascade is a key component of these inflammatory processes, there has been little research regarding its susceptibility to stress.

Methods: In experiment 1, 38 healthy participants completed an 8-minute psychological stress task. Complement components were assessed from blood samples taken by venipuncture, at rest and immediately post task. In experiment 2, 40 participants undertook a similar task; blood samples were collected from a cannula at rest, immediately post task, and after 30 and 60 minutes of recovery. In experiment 3, 40 participants were exposed to both a stress and a control session. Session order was counterbalanced and, on both occasions, we received blood samples from half the participants via a cannula and the other half by repeated venipuncture.

Results: In experiment 1, C3a levels increased significantly from rest to task, indicating complement cascade activation. In experiment 2, we found that both C3a and Factor Bb increased significantly from rest to task and recovered by 30 and 60 minutes. C5a rose significantly 30 minutes after completion of the stress task. In experiment 3, C3a increased in response to the mental stress task, whereas it decreased slightly during the control session. There was no significant effect of blood taking method.

Conclusions: These experiments demonstrate that the complement cascade is susceptible to acute psychological stress and suggest a potential mechanism for stress-induced inflammatory activation in individuals with inflammatory disorders.

Key Words: complement cascade • acute stress • inflammation

Abbreviations: PASAT = paced auditory serial addition task; RA = rheumatoid arthritis;SLE = systemic lupus erythematosus;ECG = electrocardiography;ICG = impedance cardiography;HR = heart rate;PEP = pre-injection rate;CO = cardio output;TRR = total peripheral resistance;MANOVA = multivariate repeated-measures analysis of variance;EDTA = ethylene diaminetetraacetic acid.