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The present studies examined production of the cytokines tumor necrosis factor alpha (TNF-ac), interleukin-lo (IL-1|3), and IL-6 by human monocyte-derived macrophages exposed to Pneumocystis carinii in vitro and the impact of concurrent macrophage infection with human immunodeficiency virus type 1 (HIV-1) on these cytokine responses. Macrophages were infected with the HIV-1 BaL monocytotropic strain for 10 to 14 days and then exposed to P. carinii. At various times following P. carinii treatment, culture supernatants were harvested to assess the cytokine profile. Addition of P. carinii to HIV-uninfected macrophages resulted in augmented production of IL-6, TNF-a, and IL-1" protein. By contrast, in HIV-infected macrophages exposed to P. carinii, only the release of IL-6 was increased compared with that for HIV-uninfected macrophages, while the levels of TNF-o and IL-1p decreased. This altered response was confirmed at the molecular level for TNF-ot mRNA. Preventing physical contact between P. carinii and macrophages by a membrane filter inhibited all cytokine release. Substituting P. carinii with a preparation of P. carinii 95to 115-kDa major membrane glycoprotein A yielded a response similar to that obtained by addition of intact P. carinii. These results suggest that HIV-1 infection of human macrophages modulates cytokine responses to P. carinii.

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We examined the effect of rotation-induced stress on the percentage distribution of NK-YAC-1 target-binding cells and natural killer (NK) cell activity from splenic lymphocytes of C3H/HeJ mice. Following a 6-day stress regimen, we observed a marked decline in both the percentage of target-binding cells and in NK cell activity. This decline was first evident 13 days after initiation of stress and persisted for 2 weeks. Our data indicate that intermittent rotation stress over a 6-day period results in a delayed but persistent deleterious effect on NK-YAC-1 target binding and NK cell activity.