Interestingly, BAL fluid IL-8 and PLA were elevated in asymptomatic HIV-positive patients in comparison with that in normal volunteers, and these patients had abnormal Pa02 (86 ±6.7 mm Hg) and P(A-a)02 values (26.5 ±3.6). Other investigators have demonstrated increased production of tumor necrosis factor a by alveolar macrophages from HIV-positive patients without pulmonary infections. In addition, the subgroup of patients with symptomatic NIP tended to have higher mean BAL fluid LTB4, PLA*, IL-8, and absolute neutrophil counts (not achieving statistical significance) than the subgroup of NIP patients without symptoms (data not shown). HIV infection appears to induce a continuum of incremental inflammatory changes in the lung, from asymptomatic disease with minor biochemical abnormalities to asymptomatic NIP, characterized by more profound biochemical abnormalities and the histopathologic changes of NIP (but without respiratory symptoms), to symptomatic NIP, characterized by clinical evidence of pneumonia and biochemical and histologic evidence of active inflammation. The development of overt opportunistic pulmonary infection may represent the progression of this process, as the lung succumbs to one of many infectious challenges.
The demonstration of active inflammation in the lungs of patients with AIDS-related lung disease provides a rationale for anti-inflammatory therapy for certain subgroups of these patients. The efficacy of corticosteroids in moderate to severe P carinii pneumonia exemplifies this approach. Elucidation of specific cellular or cytokine-mediated inflammatory mechanisms in particular types of pneumonitis may allow more precisely targeted anti-inflammatory measures to be employed.