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Infect Immun, May 1998, p. 1962-1967, Vol. 66, No. 5
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Involvement of T Cells in Enhanced Resistance to Klebsiella pneumoniae Septicemia in Mice Treated with Liposome-Encapsulated Muramyl Tripeptide Phosphatidylethanolamine or Gamma Interferon

Timo L. M. ten Hagen,1,* Wim van Vianen,1 Huub F. J. Savelkoul,2 Hubertine Heremans,3 Wim A. Buurman,4 and Irma A. J. M. Bakker-Woudenberg1

Department of Clinical Microbiology and Antimicrobial Therapy1 and Department of Immunology,2 Erasmus University Rotterdam, 3000 DR Rotterdam, and Department of Surgery, University of Maastricht, 6200 MD Maastricht,4 The Netherlands, and Laboratory of Immunobiology, Rega Institute, University of Leuven Medical School, B-3000 Leuven, Belgium3

Received 28 August 1997/Returned for modification 30 October 1997/Accepted 7 February 1998

We have previously shown that prophylactic administration of the liposome-encapsulated immunomodulating agents muramyl tripeptide phosphatidylethanolamine (MTPPE) and gamma interferon (IFN-gamma ) results in strongly increased survival of mice from a normally lethal septicemia with Klebsiella pneumoniae. It was anticipated that the treatment acts on macrophages and nonspecifically augments host resistance to various infections. In the present study, we provide evidence for a key role for T cells in host defense potentiation by the liposomal immunomodulators toward K. pneumoniae septicemia. It is shown that both CD4 and CD8 cells are important in immunomodulation, most likely due to production of IFN-gamma . Depletion of circulating IFN-gamma resulted in strong reduction of the antimicrobial host defense activation. Administration of interleukin-10 resulted in decreased antimicrobial host defense activation by liposomal immunomodulators. Moreover, administration of liposomal immunomodulators was shown to induce predominantly T-helper type 1 (Th1) cell populations in the spleen. These findings indicate that immunomodulation with liposomal MTPPE and IFN-gamma favors Th1 and NK cell activation.

* Corresponding author. Present address: Department of Surgical Oncology, University Hospital Rotterdam/Daniel den Hoed Cancer Center, P.O. Box 5201, 3008 AE Rotterdam, The Netherlands. Phone: 31 10 408 7682. Fax: 31 10 436 9140. E-mail: tenhagen{at}heel.fgg.eur.nl.

Infect Immun, May 1998, p. 1962-1967, Vol. 66, No. 5
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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