In bronchial epithelial and smooth muscle cells in mice, C3aR has been reported to be increased during conditions of endotoxemia [39], whereas plasma concentration of IL-1β was significantly elevated in C3aR−/− mice following LPS application, indicating that C3aR act as an anti-inflammatory receptor by attenuating LPS-induced proinflammatory cytokine production [40]. This evidence concerns the gene C3AR1 and serum lipopolysaccharide activity.