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The most frequent pathogen that causes bacterial meningitis is the Gram-positive bacterium  Streptococcus pneumoniae . By entering the brain, host cells will be activated and proinflammatory cytokines like interleukin-6 (IL-6) and tumor necrosis factor- α  (TNF- α ) are released. The goal of the current study was to examine the interaction between IL-6 and TNFR1 as receptor for TNF- α  and the innate immune response in vivo in a model of  Streptococcus pneumoniae -induced meningitis. For the experiments IL-6 −/− , TNFR1 −/− , and TNFR1-IL-6 −/−  KO mice were used. Our results revealed higher mortality rates and bacterial burden after infection in TNFR1 −/− , IL-6 −/− , and TNFR1-IL-6 −/−  mice and a decreased immune response including lower neutrophil infiltration in the meninges of TNFR1 −/−  and TNFR1-IL-6 −/−  mice in contrast to IL-6 −/−  and wild type mice. Furthermore, the increased mortality of TNFR1 −/−  and TNFR1-IL-6 −/−  mice correlated with decreased glial cell activation compared to IL-6 −/−  or wild type mice after pneumococcal meningitis. Altogether, the results show the importance of TNFR1 and IL-6 in the regulation of the innate immune response. The lack of TNFR1 and IL-6 results in higher mortality by weakened immune defence, whereas the lack of TNFR1 results in more severe impairment of the innate immune response than the lack of IL-6 alone.

mediators of inflammation

Lack of Proinflammatory Cytokine Interleukin-6 or Tumor Necrosis Factor Receptor-1 Results in a Failure of the Innate Immune Response after Bacterial Meningitis