We examined the in vitro release of
interleukin 8 (IL-8),
interleukin 10 (IL-10), and
interleukin 12 (IL-12) by alveolar macrophages from normal volunteers and HIV-1-infected subjects. Normal volunteers had very low levels of
IL-8 and
IL-10 and undetectable
IL-12 in the cell-free bronchoalveolar lavage fluid (BALF). Asymptomatic HIV-1-infected subjects had elevated levels of
IL-8 and
IL-10 in their BALF, and HIV-1-infected subjects with nonspecific
interstitial pneumonitis (NIP) or infected with Pneumocystis carinii had the highest BALF levels of
IL-10 and
IL-8. It was found that alveolar macrophages from asymptomatic HIV-1 subjects and from NIP subjects spontaneously released elevated
IL-8,
IL-10, and
IL-12. However,
AIDS subjects infected with P. carinii had cells that released elevated levels of
IL-10 and
IL-8, but low levels of
IL-12. When alveolar macrophages were stimulated with Staphylococcus aureus Cowan (SAC), cells from normal volunteers responded with a considerably increased release of
IL-8,
IL-10, and
IL-12; cells from HIV-1-infected subjects without P. carinii
infection responded with a moderate increase in release of all three
monokines. SAC stimulation did not enhance the release of
monokines by cells from
AIDS subjects with P. carinii
infection, and
IL-12 levels remained low. There was no strict relationship between spontaneous
cytokine release and p24 HIV-1
antigen expression by alveolar macrophages. Finally, we showed that neutralizing
IL-10 production by alveolar macrophages from
AIDS subjects substantially increased
IL-12 releasability.(ABSTRACT TRUNCATED AT 250 WORDS)