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TNF- hyper-responses to Gram-negative and Gram-positive bacteria in Propionibacterium acnes primed or Salmonella typhimurium infected mice

Max-Planck-Institut für Immunbiologie, Freiburg, Germany

Marina Gumenscheimer

Max-Planck-Institut für Immunbiologie, Freiburg, Germany

Chris Galanos

Max-Planck-Institut für Immunbiologie, Freiburg, Germany

Marina A. Freudenberg

Max-Planck-Institut für Immunbiologie, Freiburg, Germany, freudenberg{at}immunbio.mpg.de

IFN--dependent hypersensitivity to LPS is inducible in mice by infection or pre-treatment with killed bacteria. Hypersensitive mice exhibit enhanced inflammatory responses to LPS, including the overproduction of TNF-. Using Lpsⁿ BALB/c and Lps^d BALB/c/l mice, primed with Propionibacterium acnes or infected with Salmonella typhimurium, we show that concurrently to hypersensitivity to LPS, a hypersensitivity to other constituents of killed Gram-negative or Gram-positive bacteria and to staphylococcal enterotoxin B (SEB) develops. The TNF- hyper-responses in sensitized mice induced by different Gram-positive bacteria, are generally weaker than those by Gram-negative bacteria and vary significantly, due to the absence of a common, LPS-equivalent component. Using IFN-R^—/— and the respective wild-type mice, we demonstrate that although sensitization to LPS and killed Listeria monocytogenes is exclusively IFN--dependent, an IFN--independent, moderate sensitization to certain TNF--inducing constituents in bacteria may develop in parallel.

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