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Originally published online as doi:10.1189/jlb.0403137 on August 1, 2003

Published online before print August 1, 2003
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(Journal of Leukocyte Biology. 2003;74:966-970.)
© 2003 by Society for Leukocyte Biology

A key role of C5a/C5aR activation for the development of sepsis

Niels C. Riedemann, Ren-Feng Guo and Peter A. Ward1

Department of Pathology, University of Michigan Medical School, Ann Arbor

1 Correspondence: Department of Pathology, University of Michigan Medical School, 1301 Catherine Road, Ann Arbor, MI 48109-0602. E-mail: pward{at}umich.edu

In recent studies, evidence has been provided for complement activation early during the onset of experimental sepsis. Excessive production of the anaphylatoxin C5a thereby appears to elicit various harmful effects. Blockade of C5a or C5a receptor (C5aR) at the start of experimental sepsis has been demonstrated to greatly improve survival in rodents. There is evidence that C5a, during the onset of sepsis, enhances the production of various proinflammatory mediators in different cell types. Besides its known, other proinflammatory effects, recent work suggested an inhibitory role of C5a for innate-immune functions of phagocytic cells (phagocytosis, reactive oxygen species production, chemotaxis) during experimental sepsis. This review article provides an overview of the important role of C5a/C5aR activation for the onset and development of sepsis.

Key Words: inflammation • complement • cytokines • LPS • innate immunity • antibody




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