{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T12:44:53Z","timestamp":1789908293974,"version":"4.0.1"},"reference-count":48,"publisher":"Hindawi Limited","license":[{"start":{"date-parts":[[2016,1,1]],"date-time":"2016-01-01T00:00:00Z","timestamp":1451606400000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Mediators of Inflammation"],"published-print":{"date-parts":[[2016]]},"abstract":"<jats:p>The most frequent pathogen that causes bacterial meningitis is the Gram-positive bacterium<jats:italic>Streptococcus pneumoniae<\/jats:italic>. By entering the brain, host cells will be activated and proinflammatory cytokines like interleukin-6 (IL-6) and tumor necrosis factor-<jats:italic>\u03b1<\/jats:italic>(TNF-<jats:italic>\u03b1<\/jats:italic>) are released. The goal of the current study was to examine the interaction between IL-6 and TNFR1 as receptor for TNF-<jats:italic>\u03b1<\/jats:italic>and the innate immune response in vivo in a model of<jats:italic>Streptococcus pneumoniae<\/jats:italic>-induced meningitis. For the experiments IL-6<jats:sup>\u2212\/\u2212<\/jats:sup>, TNFR1<jats:sup>\u2212\/\u2212<\/jats:sup>, and TNFR1-IL-6<jats:sup>\u2212\/\u2212<\/jats:sup>KO mice were used. Our results revealed higher mortality rates and bacterial burden after infection in TNFR1<jats:sup>\u2212\/\u2212<\/jats:sup>, IL-6<jats:sup>\u2212\/\u2212<\/jats:sup>, and TNFR1-IL-6<jats:sup>\u2212\/\u2212<\/jats:sup>mice and a decreased immune response including lower neutrophil infiltration in the meninges of TNFR1<jats:sup>\u2212\/\u2212<\/jats:sup>and TNFR1-IL-6<jats:sup>\u2212\/\u2212<\/jats:sup>mice in contrast to IL-6<jats:sup>\u2212\/\u2212<\/jats:sup>and wild type mice. Furthermore, the increased mortality of TNFR1<jats:sup>\u2212\/\u2212<\/jats:sup>and TNFR1-IL-6<jats:sup>\u2212\/\u2212<\/jats:sup>mice correlated with decreased glial cell activation compared to IL-6<jats:sup>\u2212\/\u2212<\/jats:sup>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.<\/jats:p>","DOI":"10.1155\/2016\/7678542","type":"journal-article","created":{"date-parts":[[2016,1,28]],"date-time":"2016-01-28T21:02:31Z","timestamp":1454014951000},"page":"1-12","source":"Crossref","is-referenced-by-count":30,"title":["Lack of Proinflammatory Cytokine Interleukin-6 or Tumor Necrosis Factor Receptor-1 Results in a Failure of the Innate Immune Response after Bacterial Meningitis"],"prefix":"10.1155","volume":"2016","author":[{"given":"Lea-Jessica","family":"Albrecht","sequence":"first","affiliation":[{"name":"Department of Anatomy and Cell Biology, RWTH Aachen University, 52074 Aachen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Simone C.","family":"Tauber","sequence":"additional","affiliation":[{"name":"Department of Neurology, RWTH 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