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Cytokines are suspected of playing an important role in the pathophysiology of septic shock. This study was undertaken to determine whether tumor necrosis factor alpha (TNF-a) induces the production of other cytokines and mediates mortality in a neonatal rat model of sepsis caused by group B streptococci (GBS). We have measured TNF-a, interleukin-la (IL-1a), interleukin-6 (IL-6), and gamma interferon (IFN-y) levels in neonatal rats infected with different strains (H738, 259, and 90) and doses (1 50% lethal dose [LD50] and 5 90% lethal doses [LD,0]) of type III GBS. TNF-ca and IL-6 were detected by the L929 cytotoxicity and the B9 proliferation assays, respectively, in serial plasma samples. IL-la and IFN-y were measured in spleen homogenates by enzyme-linked immunosorbent assay kits by using antibodies raised against the corresponding mouse cytokines. Plasma TNF-a levels significantly rose above baseline values within 12 h after intraperitoneal challenge with 5 LD90 of GBS strain H738, corresponding to 3 x 103 CFU. A mean peak TNF-a concentration of 232 + 124 U/ml was reached at 20 h. Peak IL-la and IL-6 levels of 766 404 U/g and 1,033 + 520 U/ml, respectively, were reached at 24 h after bacterial challenge. Maximal spleen concentrations of IFN-y (449 283 U/g) were measured at 36 h. Concentrations of TNF-a, but not other cytokines, remained significantly elevated at 72 h, a time when mortality approached 100%o. Significant correlations were found between concentrations of each of the cytokines tested and the logs of CFU concentrations in the blood. In order to ascertain whether TNF-a influenced the production of other cytokines, rat pups received two in,jections of anti-murine TNF-a or normal rabbit serum at 2 h before and at 26 h after challenge with live GBS. Plasma TNF-a bioactivity was undetectable in anti-TNF-a-treated animals, while IL-6 and IFN-y, but not IL-1a, levels were significantly reduced, compared with normal serum controls. Rat pups pretreated with anti-TNF-a serum and infected with 1 and 5 LD90 of strains H738 and 259 showed enhanced early (48 to 72 h) survival.
Cytokines are suspected of playing an important role in the pathophysiology of septic shock. This study was undertaken to determine whether tumor necrosis factor alpha (TNF-a) induces the production of other cytokines and mediates mortality in a neonatal rat model of sepsis caused by group B streptococci (GBS). We have measured TNF-a, interleukin-la (IL-1a), interleukin-6 (IL-6), and gamma interferon (IFN-y) levels in neonatal rats infected with different strains (H738, 259, and 90) and doses (1 50% lethal dose [LD50] and 5 90% lethal doses [LD,0]) of type III GBS. TNF-ca and IL-6 were detected by the L929 cytotoxicity and the B9 proliferation assays, respectively, in serial plasma samples. IL-la and IFN-y were measured in spleen homogenates by enzyme-linked immunosorbent assay kits by using antibodies raised against the corresponding mouse cytokines. Plasma TNF-a levels significantly rose above baseline values within 12 h after intraperitoneal challenge with 5 LD90 of GBS strain H738, corresponding to 3 x 103 CFU. A mean peak TNF-a concentration of 232 + 124 U/ml was reached at 20 h. Peak IL-la and IL-6 levels of 766 404 U/g and 1,033 + 520 U/ml, respectively, were reached at 24 h after bacterial challenge. Maximal spleen concentrations of IFN-y (449 283 U/g) were measured at 36 h. Concentrations of TNF-a, but not other cytokines, remained significantly elevated at 72 h, a time when mortality approached 100%o. Significant correlations were found between concentrations of each of the cytokines tested and the logs of CFU concentrations in the blood. In order to ascertain whether TNF-a influenced the production of other cytokines, rat pups received two in,jections of anti-murine TNF-a or normal rabbit serum at 2 h before and at 26 h after challenge with live GBS. Plasma TNF-a bioactivity was undetectable in anti-TNF-a-treated animals, while IL-6 and IFN-y, but not IL-1a, levels were significantly reduced, compared with normal serum controls. Rat pups pretreated with anti-TNF-a serum and infected with 1 and 5 LD90 of strains H738 and 259 showed enhanced early (48 to 72 h) survival.
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