This Article Full Text (PDF) References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Merlin, T. Articles by Freudenberg, M. A. Search for Related Content PubMed PubMed Citation Articles by Merlin, T. Articles by Freudenberg, M. A. Social Bookmarking                         What's this?

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.

Journal of Endotoxin Research, Vol. 7, No. 2, 157-163 (2001)
DOI: 10.1177/09680519010070021001


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?