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Role of interferons in LPS hypersensitivity

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

Christoph Kalis

Max-Planck-Institut für Immunbiologie, Freiburg, Germany

Yolande Chvatchko

Serono Pharmaceutical Research Institute, Plan-les-Ouates, Geneva, Switzerland

Thomas Merlin

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

The innate immune response to Gram-negative bacteria depends mainly on the ability of the host to respond to the LPS component. Consequently, the state of LPS sensitivity at the time of infection and the numbers of invading bacteria (i.e. the amounts of LPS) are primary factors determining the innate responses provoked by Gram-negative pathogens. LPS sensitivity increases following treatment of mice with live or killed micro-organisms. Two types of sensitization have been recognized, strong, IFN--dependent and moderate IFN--independent. IL-12 and IL-18 are intimately involved in the induction of IFN- by bacteria. We showed that Gram-negative bacteria induce IFN- in mice also by an IFN-ß-dependent pathway that requires IL-18 and is independent of IL-12 signaling. This pathway is STAT4 dependent, the activation of which is directly linked to IFN-ß. Further, IFN-ß can be replaced by IFN-. While different components of Gram-negative bacteria induce IL-12 and IL-18, LPS seems to be the only component in these bacteria capable of inducing IFN-ß. Therefore, the IFN-ß pathway of IFN- induction, unlike the IL-12 pathway, proceeds only in LPS responder mice. The IFN-/ß-dependent pathway is expected to play a role whenever IFN- or IFN-ß, and IL-18 are produced concomitantly during infection.

Journal of Endotoxin Research, Vol. 9, No. 5, 308-312 (2003)
DOI: 10.1177/09680519030090050601


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