Alveolar macrophage and glycoprotein responses to Pneumocystis carinii

Pneumocystis carinii continues to represent an important complication of immunosuppression in patients with acquired immune deficiency syndrome, hematological and solid malignancies, organ transplantation, and during corticosteroid and cytotoxic therapy for inflammatory disorders. Although host defenses against this organism center around CD4 lymphocytic function, additional immune mediators in the alveolar spaces contribute substantially to host recognition and elimination of P carinii. In particular, this review considers the interactions of P carinii with alveolar macrophages, adhesive glycoproteins including vitronectin and fibronectin, and surfactant lipids and protein components. Recent studies indicate that alveolar macrophages contribute significantly to host responses against this organism by mediating uptake and degradation of P carinii, and by releasing inflammatory mediators including reactive oxidants, eicosanoids, and the potent proinflammatory cytokine tumor necrosis factor-α. Furthermore, the interactions of P carinii with multiple adhesive proteins and with surfactant components additionally modulate the interactions of P carinii with macrophages and enhance host recognition of this pathogen. These non-lymphocytic mediators represent additional important mechanisms of host recognition and response to P carinii infection.