ABSTRACT
A recent series of investigations using animal models of allergic airways disease as well as correlative studies in human asthmatics have suggested that C3a and C5a anaphylatoxins are significant mediators of inflammation in the airways. Receptors for the anaphylatoxins are present in airway epithelium and upregulated in the presence of inflammation. The C3a receptor is also present on airway smooth muscle. In this chapter we will briefly review the pathways leading to complement activation, the animal models implicating a role for C3a and C5a in asthma, and the clinical studies that correlate asthma with complement activation. The development of small molecule antagonists for the C3a and C5a receptors, which has finally been achieved, may soon allow for a proof-of-concept trial in human disease.
