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Infection and Immunity, December 2001, p. 7271-7276, Vol. 69, No. 12
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.12.7172-7276.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Differences in Innate Defense Mechanisms in Endotoxemia and Polymicrobial Septic Peritonitis

Bernd Echtenacher,1 Marina A. Freudenberg,2 Robert S. Jack,3 and Daniela N. Männel3,*

Max-Planck-Institute for Immunobiology, Freiburg,1 Institute for Immunology, University of Greifswald, Greifswald,2 and Institute for Pathology/Tumor Immunology, University of Regensburg, Regensburg,3 Germany

Received 8 June 2001/Returned for modification 13 July 2001/Accepted 20 August 2001

Loss, reduction, or enhancement of the ability to respond to bacterial lipopolysaccharide (LPS) has no influence on survival of mice in a model of postoperative polymicrobial septic peritonitis induced by cecal ligation and puncture (CLP). This was demonstrated by using either mice with a defective Tlr4 gene, which encodes the critical receptor molecule for LPS responses, or mice deficient for LPS binding protein (LBP) or mice sensitized to LPS by Propionibacterium acnes. Though interleukin-12 (IL-12) and gamma interferon (IFN-gamma ) play an important role in the sensitivity to LPS as well as in the resistance to several infections, loss of these cytokine pathways does not affect survival after CLP. Thus, neutralization of neither endogenous IL-12 nor IFN-gamma altered mortality. In addition, IFN-gamma receptor-deficient mice demonstrated the same sensitivity to CLP as mice with a functional IFN-gamma receptor. However, administration of IFN-gamma at the time of operation or pretreatment of both IFN-gamma -sensitive and IFN-gamma -resistant mice with IL-12 significantly enhanced mortality. This indicates that in the present infection model activation of innate defense mechanisms is not dependent on LPS recognition and does not require endogenous IL-12 or IFN-gamma function. Indeed, exogenous application of these two mediators had deleterious effects.

* Corresponding author. Mailing address: Institute of Pathology/Tumor Immunology, University of Regensburg, F.-J.-Strauss-Allee, D-93042 Regensburg, Germany. Phone: 49.941.944-6622. Fax: 49.941.944-6602. E-mail: daniela.maennel{at}klinik.uni-regensburg.

Infection and Immunity, December 2001, p. 7271-7276, Vol. 69, No. 12
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.12.7172-7276.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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