Abstract
In order to elucidate the role played by alveolar cytokines in the pathogenesis of HIV-related lung damage, levels of interleukin (IL) 1ß, IL-2, IL-6, tumor necrosis factor (TNF)-$aL, and interferon (Ifn) were assessed on supernatant of bronchoalveolar lavage fluid from 30 consecutive HIV-1 seropositive (HIVAb+) patients with clinical and radiologic evidence of pneumonia, from 20 HIV— seronegative (HIVAb—) patients with pulmonary sarcoidosis, and from 10 HIVAb— healthy control subjects. Cytokine levels were expressed as picogram (IL-1, TNF), nanogram (IL-6), and international unit (IL-2, Ifn) per milligram of albumin per deciliter. Total and differential cell counts, cytofluorimetric enumeration of CD3+, CD3+/DR+, CD4+, CD8+, and CD8+/CD16+ cells, as well as microbiologic investigations for opportunistic agents were performed on lavage pellets. HIV-related pneumonia was characterized by higher mean alveolar level of IL-2 (12 ±5 IU), and by more elevated mean counts of T cells (109 ± 16), activated T cells (60 ± 12), and CD8+ cells (90 ± 13)/µ l if compared with both active sarcoidosis and control subjects, where respective values of 0.2±0.1 and 0.3±0.2 IU IL-2/mgAlb/dl, of 52±11 and 7±2 T cells, of 20±5 and 1.2±0.3 activated T cells, and of 11 ±2 and 3 ±0.6 CD8+ cells per microliter were found. HIV-infected patients with opportunistic lung infections (OIs) showed the highest mean IL-2 level (21 ±4 IU), and higher counts of both CD8+ (117 ±20) and CD8+/CD16+ (36 ±7) cells per microliter if compared with patients without evidence of OIs (respectively, 62 ±13 CD8+ and 18 ±3 CD8+/CD16+ cells per microliter). By contrast, extremely high IL-1 levels (1,463 ±760 pg), and IL-2 levels similar to control subjects (3.4 ± 1.2 IU), were found in the absence of OIs. Different mechanisms depending respectively on IL-2-mediated cytotoxic cell recruitment and activation, or IL-1-mediated tissue injury may account for HIV-related lung damage, depending on the presence or absence of opportunistic agents.
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