• Markus Huber-Lang, J Vidya Sarma, Daniel Rittirsch, Heike Schreiber, Manfred Weiss, Michael Flierl, Ellen Younkin, Marion Schneider, Heidemarie Suger-Wiedeck, Florian Gebhard, Shannon D McClintock, Thomas Neff, Firas Zetoune, Uwe Bruckner, Ren-Feng Guo, Peter N Monk, and Peter A Ward.
• Department of Traumatology, Hand and Reconstructive Surgery, University of Ulm Medical School, Germany.
• J. Immunol. 2005 Jan 15;174(2):1104-10.

AbstractSepsis is associated with extensive complement activation, compromising innate immune defenses, especially in neutrophils (PMN). Recently, a second C5a receptor (C5L2) was detected on PMN without evidence of intracellular signaling. The current study was designed to determine changes in C5L2 in blood PMN during sepsis. In vitro exposure of PMN to C5a, but not to fMLP, led to reduced content of C5L2. Following cecal ligation and puncture-induced sepsis in rats, PMN demonstrated a time-dependent decrease in C5L2. In vivo blockade of C5a during experimental sepsis resulted in preservation of C5L2. Similarly, PMN from patients with progressive sepsis showed significantly reduced C5L2 expression (n = 26), which was virtually abolished in patients who developed multiorgan failure (n = 10). In contrast, sepsis survivors exhibited retention of C5L2 (n = 12/13). The data suggest that C5L2 on PMN diminishes during sepsis due to systemic generation of C5a, which is associated with a poor prognosis.

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