Asthma and the acute response distress syndrome (ARDS) are two of the more well-known examples of dysregulated complement activation. It is now well established from both experimental models of sepsis and clinical studies in humans that the complement system plays a key role in the pathophysiology of asthma and the acute respiratory distress syndrome (reviewed in Wills-Karp 2007; Sarma et al. 2006) . Asthma is a chronic inflammatory upper airway disease with increasing prevalence throughout the world and especially in young children in the developed world. In asthma, hyper-secretion of mucus occurs in the airways along with smooth muscle proliferation in upper airway (bronchial/bronchiolar) walls together with increased numbers of mast cells, CD4+ T cells and eosinophils. This leads to obstructed airways and accentuated upper airway contractile responses leading to shortness of breath, wheezing and coughing. In ARDS, there is a severe impairment of gas exchange due to damage to the alveolar and vascular epithelium resulting in increased permeability of plasma contents and influx of neutrophils into the interstitial and alveolar spaces.