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Infection and Immunity, September 2002, p. 4805-4811, Vol. 70, No. 9
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.9.4805-4811.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Comparison of Host Resistance to Primary and Secondary Listeria monocytogenes Infections in Mice by Intranasal and Intravenous Routes

Mayuko Mizuki,1 Akio Nakane,1* Kenji Sekikawa,2 Yoh-ich Tagawa,3 and Yoichiro Iwakura4

Department of Bacteriology, Hirosaki University School of Medicine, Hirosaki,1 Department of Molecular Biology and Immunology, National Institute of Agrobiological Sciences, Tsukuba,2 Institute of Experimental Animals, Shinshu University School of Medicine, Matsumoto,3 Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, Tokyo, Japan4

Received 18 March 2002/ Returned for modification 23 April 2002/ Accepted 23 May 2002

There have been no studies on the susceptibility and host immune responses to an intranasal infection with Listeria monocytogenes. In this study, we compared the susceptibilities and cytokine responses between intranasal and intravenous infections with L. monocytogenes in mice. Moreover, we compared efficiency of acquisition of host resistance to L. monocytogenes infection between intranasally and intravenously immunized mice because an intranasal immunization of vaccines is reportedly available for induction of adaptive immunity against various infectious pathogens. The susceptibility to an intranasal infection with L. monocytogenes was markedly lower than that to the intravenous infection. The bacterial growth in the lungs, spleens, and livers was substantially similar between intranasally and intravenously infected mice. Titers of endogenous gamma interferon (IFN-{gamma}) and tumor necrosis factor-{alpha} (TNF-{alpha}) in the spleens, livers, and lungs were parallel to bacterial numbers in each organ of mice during intranasal infection and intravenous infection. IFN-{gamma}-deficient mice and TNF-{alpha}-deficient mice were highly susceptible to intranasal infection as well as intravenous infection. Susceptibilities to intranasal and intravenous L. monocytogenes infection were the same in these cytokine-deficient mice. These results suggest that both IFN-{gamma} and TNF-{alpha} play critical roles in host resistance to intranasal L. monocytogenes infection as well as the intravenous infection. Acquisition of host resistance to intravenous and intranasal L. monocytogenes infection was induced in intranasally immunized mice as well as intravenously immunized mice, suggesting that intranasal immunization is effective for prevention of a systemic infection with L. monocytogenes.

* Corresponding author. Mailing address: Department of Bacteriology, Hirosaki University School of Medicine, Zaifu-cho 5, Hirosaki, Aomori 036-8562, Japan. Phone: 81-172 39-5032. Fax: 81-172 39-5034. E-mail: a27k03n0{at}cc.hirosaki-u.ac.jp.

Editor: D. L. Burns

Infection and Immunity, September 2002, p. 4805-4811, Vol. 70, No. 9
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.9.4805-4811.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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