“…As reported in other asthma models, C3a and C5a participate in shifting Th2 and Th1 balance respectively but blocking or antagonizing C5a shift response to Th2 [13] and Th2 shift results in elevated Th2 adaptive response followed by airway inflammation [42]. These anaphylatoxins can induce ASM contraction [20, 58, 59], mucus secretion [60, 61], increased microvascular permeability [62, 63] [17, 24], vasodilation [64, 65], leukocyte migration and activation, and degranulation of mast cells [66], which are the hallmarks features of asthma. Further, the most important, neutralization of anaphylatoxin activity through the use of blocking antibodies, genetic targeting or by using specific antagonist of various complement factors or their receptors has been shown to attenuate allergic inflammation, and AHR in mice, and guinea pigs [67, 68].…”