IL-10 in Antilipopolysaccharide Immunity Against Systemic Klebsiella Infections

Aim. This study was undertaken in order to determine whether anti-inflammatory cytokine interleukin-10 is responsible for a previously described protection against Klebsiella infection mediated by antilipopolysaccharide antibodies. Methods. BALB/c mice were infected intraperitoneally with a lethal challenge of Klebsiella pneumoniae Caroli. One group was protected with monoclonal antibodies prior to infection and the second was not. We measured plasma levels of interleukin-10 at different time points by enzyme immunoassay and analyzed the relation between interleukin-10 and proinflammatory cytokines interleukin-6 and tumor necrosis factor-α in order to determine the association of these ratios with the outcome of infection. Major findings and conclusions. We found different pattern of interleukin-10 production in protected mice compared with unprotected ones. The difference is greatest 24 hours postinfection. The ratios between IL-10 and proinflammatory cytokines confirmed the suppressed proinflammatory response in protected animals, especially 24 hours postinfection. Hence the mortality in unprotected mice begins immediately after we conclude that such cytokine relation and IL-10 production are, at least partially, responsible for the destiny of infected animals and the outcome of infection

Proinflammatory Cytokines in Antilipopolysaccharide Immunity Against Klebsiella Infections

This study was undertaken in order to determine whether proinflammatory cytokines are involved in a previously described protection against Klebsiella infection mediated by antilipopolysaccharide antibodies. BALB/c mice were infected intraperitoneally with a lethal challenge of Klebsiella pneumoniae Caroli. One group of mice was protected with monoclonal antibodies against lipopolysaccharide prior to infection and the second was not. We determined the number of colony-forming units at different time points in the blood of infected animals and paralleled them with plasma levels of five proinflammatory cytokines measured by enzyme immunoassays. Our results show that the two groups of animals tested expressed different plasma concentrations for all cytokines. The greatest difference was detected 24 hours after infection, with a higher production in the unprotected group. We concluded that a reduced cytokine production is partially responsible for the survival of protected animals