Interleukin (IL)-6 and -8 are important inflammatory cytokines in bacterial infections. Their serum and urine concentrations were measured in 27 neonates with urinary tract infection (UTI) at onset and the second week of therapy, as well as in 23 control neonates. Escherichia coli was isolated in 89% of cases. 99mTc-dimercaptosuccinic acid (99mTc-DMSA) scans were performed between the 10th and 90th days after UTI and showed pyelonephritic changes in 15 neonates (56%). Increased IL-6 and IL-8 concentrations were found in urine but not in serum within the first 24 h after presumptive diagnosis of UTI (P=.036 and.010, respectively), suggesting that the neonatal urinary tract can respond to uropathogens by producing inflammatory cytokines. Urine concentrations of IL-6 correlated with findings of renal changes in 99mTc-DMSA scans (P=.012) and thus may serve as a marker of renal parenchymal outcome. All neonates exhibited undetectable urine cytokine levels during the second week of therapy.
The effects of interleukin (IL)-10, a potent antiinflammatory cytokine, on human monocyte functions against two medically important pathogens, Candida albicans and Staphylococcus aureus, were studied. Incubation with 20-100 ng/mL IL-10 for 2-3 days decreased the fungicidal activity of monocytes against serum-opsonized C. albicans blastoconidia (P=.04), reduced their capacity to damage unopsonized hyphae (P=.006), and suppressed superoxide anion production in response to phorbol myristate acetate (P=.019) and N-FMLP (P=.04) but not to serum-opsonized blastoconidia. Paradoxically, IL-10 enhanced phagocytic activity of monocytes against serum-opsonized blastoconidia (P<.01). In addition, IL-10-treated monocytes demonstrated decreased bactericidal activity (P=.046) but no change in bacterial phagocytosis. These findings demonstrate an overall suppressive role of IL-10 on human monocyte function against C. albicans and S. aureus and may have important implications in the use of this cytokine.
The potential of recombinant human interleukin-12 (IL-12) to enhance the capacity of human monocytes (MNC) to elicit an oxidative burst and damage hyphae of Aspergillus fumigatus was investigated. Incubation of peripheral blood mononuclear cells (PBMC) from healthy adults with 10 to 100 ng of IL-12/ml at 37°C for 2 to 3 days enhanced the production of superoxide anion (O2
−) in response to phorbol myristate acetate (PMA) (P = 0.04) and unopsonized A. fumigatus hyphae (P = 0.03) and further enhanced hyphal damage (P = 0.009). Anti-gamma interferon (anti-IFN-γ) blocked secretion of IFN-γ by IL-12-treated PBMC but did not inhibit IL-12-induced O2
− production by these cells in response to PMA. In addition, IL-12-treated elutriated MNC secreted no IFN-γ or tumor necrosis factor alpha but exhibited enhanced O2
− production compared to controls (P = 0.013). These findings demonstrate that IL-12 augments oxidative antifungal activities of MNC via an IFN-γ-independent route, suggesting a novel pathway of IL-12 action in antifungal defense.
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