That PLAg, but not LTB4, was significantly elevated in patients with P carinii pneumonia suggests that while LTB4 does not play a role in the lung injury of P carinii pneumonia, other products of PLAa action (eg, lysophospholipids and free fatty acids) may contribute to pulmonary dysfunction. Elevation of PLAa levels in P carinii pneumonia provides both a mechanism for the lung injury seen in this disease and a corticosteroid-sensitive therapeutic target.
BAL fluid LTB4, PLAg, and IL-8 were elevated in patients with NIP IL-8 levels correlated with the P(A-a)02 in these patients, while the LTB4 and PLA2 levels correlated with the absolute neutrophil count. These data suggest that both LTB4 and IL-8 contribute to the pathogenesis of lung injury in NIP Nonspecific interstitial pneumonitis appears to be a common cause of respiratory symptoms in patients with AIDS. It does not represent occult P carinii pneumonia; HIV itself, other viral infections, immune complexes, and previous opportunistic infections have been suggested as possible causes. Recent evidence indicates that HIV infection of pulmonary lymphoid cells may play a role in the pathogenesis of NIP The presence of active inflammation, as indicated by elevated BAL fluid LTB4, PLA2, and IL-8, suggests a dynamic, ongoing process. These findings may reflect the biochemical and pathologic consequences of constant challenges by viruses, bacteria, and opportunistic pathogens.