Unlike viruses, bacteria are attacked by immune proteins known as complement proteins when they enter the circulation. Complement proteins are involved in kill­ing bacteria through three pathways: the classical complement pathway, the alterna­tive complement pathway, and the lectin pathway. The rst step of the classical complement pathway requires antibodies to bind to the surface of the target bacte­ria. The antibodies are then targeted by a specic complement protein complex. Once bound, it initiates the disassembly and remodeling of complement complexes that produce opsonins that tag bacteria for destruction. At the end of this pathway, the membrane attack complex (MAC) is formed. MAC can localize to Gram­negative bacteria cell membranes, but not to Gram-positive bacteria cell mem­branes. This process produces pores that facilitate the entry of membrane-damaging molecules such as lysozyme into bacteria, making them susceptible to osmotic lysis. The alternative complement pathway does not require antibodies. In this path­way, complement proteins of a complex known as C3 bind directly to bacteria and activate downstream components of the complement cascade. This results in the formation of MAC, which causes lysis of the bacteria. During the lectin pathway, mannan-binding lectin (MBL) attaches to proteins containing mannose residues found in some bacterial species [24]. The importance of complement in defense against respiratory infections is recapitulated by the clinical features of patients with primary complement deciencies [25].