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Infection and Immunity, April 2000, p. 1988-1996, Vol. 68, No. 4
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Purified Lipopolysaccharide from Francisella tularensis Live Vaccine Strain (LVS) Induces Protective Immunity against LVS Infection That Requires B Cells and Gamma Interferondagger

Valley C. Dreisbach,1 Siobhan Cowley,2,Dagger and Karen L. Elkins1,*

Laboratory of Mycobacteria, Division of Bacterial Products, Center for Biologics Evaluation and Research, Food and Drug Administration, Rockville, Maryland 20852,1 and Department of Biochemistry and Microbiology, University of Victoria, Victoria, British Columbia, Canada V8W 3P62

Received 11 November 1999/Returned for modification 29 December 1999/Accepted 13 January 2000

Previous results have demonstrated that nonspecific protective immunity against lethal Francisella tularensis live vaccine strain (LVS) or Listeria monocytogenes infection can be stimulated either by sublethal infection with bacteria or by treatment with bacterial DNA given 3 days before lethal challenge. Here we characterize the ability of purified lipopolysaccharide (LPS) from F. tularensis LVS to stimulate similar early protective immunity. Treatment of mice with surprisingly small amounts of LVS LPS resulted in very strong and long-lived protection against lethal LVS challenge within 2 to 3 days. Despite this strong protective response, LPS purified from F. tularensis LVS did not activate murine B cells for proliferation or polyclonal immunoglobulin secretion, nor did it activate murine splenocytes for secretion of interleukin-4 (IL-4), IL-6, IL-12, or gamma interferon (IFN-gamma ). Immunization of mice with purified LVS LPS induced a weak specific anti-LPS immunoglobulin M (IgM) response and very little IgG; however, infection of mice with LVS bacteria resulted in vigorous IgM and IgG, particularly IgG2a, anti-LPS antibody responses. Studies using various immunodeficient mouse strains, including LPS-hyporesponsive C3H/HeJ mice, µMT- (B-cell-deficient) knockout mice, and IFN-gamma -deficient mice, demonstrated that the mechanism of protection does not involve recognition through the Lpsn gene product; nonetheless, protection was dependent on B cells as well as IFN-gamma .

* Corresponding author. Mailing address: DBP/CBER/FDA, 1401 Rockville Pike, HFM 431, Bethesda, MD 20852. Phone (301) 496-0544. Fax: (301) 402-2776. E-mail: elkins{at}cber.fda.gov.

dagger This article is dedicated to the memory of Roberta D. Shahin, our friend and colleague, whose insight, encouragement, and companionship were instrumental throughout the progression of these and many other studies.

Dagger Present address: Division of Infectious Diseases, UBC and VHHSC, Department of Medicine, Vancouver, BC, Canada V5Z 3J5.

Infection and Immunity, April 2000, p. 1988-1996, Vol. 68, No. 4
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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