Mechanisms of defence in the lung: lessons from Pneumocystis carinii Pneumonia

Pneumocystis carinii continues to represent an important complication of in dividuals with compromised immunity. P. carinii interacts with immune and n on-immune cells in the lung and mediates lung injury through a variety of m echanisms. CD4+ T lymphocytes are the cornerstone in defence against P. car inii. Recent studies indicate that alveolar macrophages provide essential f unctions that significantly enhance clearance of P. carinii infection. P. c arinii also attaches to alveolar epithelial cells, causing inhibition of ep ithelial growth and replication. In addition to cellular interactions, P. c arinii organisms bind to a variety of host adhesive proteins present in the lower respiratory tract. Binding of these proteins to P. carinii modulates host cell recognition and immune responses to the parasite. During the cou rse of P. carinii pneumonia, several inflammatory mediators are produced in the lung. Although necessary for control of infection, exuberant inflammat ory responses also predispose the host to the development of acute lung inj ury. Thus, host defences against P. carinii depend on complex interactions between immune and non-immune cells as well as several mediators that facil itate host recognition and eventual elimination of infection. Understanding these complex processes may enable development of novel therapeutic approa ches for management of this important infection.