Abstract. Concentrations and ex vivo production of interleukin 1b (IL-1), tumour necrosis a (TNF), interleukin 6 (IL-6), interleukin-1 receptor antagonist (IL-1RA) and TNF soluble receptors (sTNF-receptors, P55 and P75) were measured in bronchoalveolar lavage (BAL) fluid and blood in 23 HIV-seropositive (HIV+) patients with Pneumocystis carinii pneumonia (PCP) and compared with values found in healthy HIV-seronegative (HIV-) controls and asymptomatic HIV+ subjects. Concentrations of the proinflammatory cytokine IL-1b were increased in BAL fluid of HIV+ patients with PCP (184 Ϯ 47 pg mL -1 ) compared with undetectable levels in healthy control subjects (P = 0 . 0001). In plasma of these patients higher concentrations of the anti-inflammatory cytokine IL-1RA were found during acute PCP than after recovery (2 . 1 Ϯ 0 . 7 vs. 0 . 5 Ϯ 0 . 2 ng mL -1 , P = 0 . 01). No correlations could be found between cytokine concentrations and clinical severity of the infection. Corticosteroid treatment did not influence cytokine concentrations in BAL or blood, nor did it suppress the production in alveolar cells. In whole-blood cultures, however, lipopolysaccharide (LPS)-stimulated production was significantly suppressed for IL-1 (1 . 3 vs. 5 . 5 ng mL -1 , P = 0 . 009) and for IL-6 (0 . 6 vs. 2 . 5 ng mL -1 , P = 0 . 01). The overall data show that in HIV+ patients with PCP (similar to what we had found previously in HIVpatients with PCP) proinflammatory cytokines are more prominently present in BAL, whereas anti-inflammatory reaction is predominant in the circulation.
Abstract. Concentrations and ex vivo production of interleukin-(IL-1 /?), tumour necrosis factor-a (TNF), interleukin-6 (IL-6), interleukin-1 receptor antagonist (IL-1RA) and TNF soluble receptors were followed in bronchoalveolar lavage (BAL) fluid and blood from 10 HIV -seronegative patients with Pneumocystis carinii pneumonia (PCP) and compared with values found in healthy volunteers. During the acute phase of PCP, TNF but not IL-6 or IL-1/? was detectable in BAL fluid. At that time, plasma concentrations of the proinfiammatory cyto kines were low, whereas plasma concentrations of the anti-inflammatory cytokines were high. The ex vivo production capacity of proinfiammatory cytokines was suppressed in the acute phase, in the blood as well as at the site of infection. During convalescence the production capacity of the blood cells normalized. The I.L-1RA production capacity of the alveolar cells was also suppressed in the acute phase, but preserved in blood cells.
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