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CUTTING EDGE |
*
Institute of Molecular Medicine for the Prevention of Human Diseases,
Department of Integrative Biology, Physiology, and Pharmacology, and
Department of Biochemistry and Molecular Biology, University of Texas-Houston, Houston, TX 77030
The complement anaphylatoxin C3a, on binding the C3aR, mediates
numerous proinflammatory activities. In addition, recent in vitro
studies with C3a have implicated C3aR as a possible
anti-inflammatory receptor. Because of its possible dual role in
modulating the inflammatory response, it is uncertain whether C3aR
contributes to the pathogenesis of endotoxin shock. Here, the
targeted-disruption of the C3aR in mice is reported. These mice exhibit
an enhanced lethality to endotoxin shock with a pronounced gene dosage
effect. In addition, the plasma concentration of IL-1
was
significantly elevated in the C3aR-/- mice compared with
their littermates following LPS challenge. These findings demonstrate
an important protective role for the C3aR in endotoxin shock and
indicate that, in addition to its traditionally accepted functions in
mediating inflammation, the C3aR also acts in vivo as an
anti-inflammatory receptor by attenuating LPS-induced
proinflammatory cytokine production.
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