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      Interleukin-6 gene-deficient mice show impaired defense against pneumococcal pneumonia.

      The Journal of Infectious Diseases

      immunology, Acute-Phase Proteins, analysis, Animals, Cytokines, biosynthesis, Interleukin-6, genetics, physiology, Lung, microbiology, Mice, Mice, Inbred C57BL, Pneumonia, Pneumococcal, RNA, Messenger, Receptors, Tumor Necrosis Factor, blood, Streptococcus pneumoniae, isolation & purification

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          Abstract

          Induction of pneumonia in C57Bl/6 mice by intranasal inoculation with 10(6) cfu of Streptococcus pneumoniae resulted in sustained expression of interleukin (IL)-6 mRNA in lungs and increases in lung and plasma IL-6 concentrations. In IL-6-deficient (IL-6-/-) mice, pneumonia was associated with higher lung levels of the proinflammatory cytokines tumor necrosis factor-alpha, IL-1beta, and interferon-gamma and of the antiinflammatory cytokine IL-10 than in wild type (IL-6+/+) mice (all P < .05). Also, the plasma concentrations of soluble tumor necrosis factor receptors were higher in IL-6-/- mice (P < .05), while the acute-phase protein response was strongly attenuated (P < .01). Lungs harvested from IL-6-/- mice 40 h after inoculation contained more S. pneumoniae colonies (P < .05). IL-6-/- mice died significantly earlier from pneumococcal pneumonia than did IL-6+/+ mice (P < .05). During pneumococcal pneumonia, IL-6 down-regulates the activation of the cytokine network in the lung and contributes to host defense.

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          9237710

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