The interaction of C5a with its receptors, C5aR (CD88) and C5L2, is crucial for mediating the pulmonary inflammatory response. Bronchial and alveolar epithelial cells have been shown to express the C5aR [114, 115] . Mice lacking the C5aR gene showed a decreased extent of pulmonary inflammation, as characterized by attenuated myeloperoxidase production by neutrophils and decreased vascular leakage [116] .