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Infection and Immunity, October 2002, p. 5596-5603, Vol. 70, No. 10
0019-9567/02/$04.00+0 DOI: 10.1128/IAI.70.10.5596-5603.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
Max-Planck-Institut für Immunbiologie, 79 108 Freiburg, Germany
Received 9 April 2002/ Returned for modification 6 June 2002/ Accepted 1 July 2002
Priming with heat-killed Propionibacterium acnes enhances the sensitivity of mice to lipopolysaccharide (LPS) and other biologically active bacterial components. We show that P. acnes priming has protective and deleterious effects on a subsequent serovar Typhimurium infection. It may result in a complete protection or prolonged survival, or it may accelerate mortality of the infected mice, depending on the number of serovar Typhimurium bacteria administered and on the degree of LPS hypersensitivity at the time of infection. Both effects of P. acnes-induced hypersensitivity are mediated by gamma interferon (IFN-
) and are based on a differential activation of the innate immune mechanisms which recognize and react against the LPS present in infecting bacteria. In P. acnes-primed mice null for LPS-binding protein (LBP-/- mice), the impaired LPS recognition, due to the absence of LBP, resulted in a higher resistance to serovar Typhimurium infection. A similar P. acnes priming of mice had a protective, but no deleterious effect on a subsequent L. monocytogenes infection. This effect was IFN-
dependent but independent of LBP.
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