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a The Center for Microbial Interface Biology; Department of Molecular Virology, Immunology and Medical Genetics; and Department of Internal Medicine, Division of Infectious Diseases, The Ohio State University, Columbus, OH 43210, USA b Department of Medicine, Division of Allergy and Infectious Diseases, University of Washington, HSB T-293, Box 357710, 1959 NE Pacific Street, Seattle, WA 98195, USA
Key Words: LPS • lipopolysaccharide • gray variant • phase variation • LPS modification • LPS structure • lipid A • O-antigen
Address for correspondence: John S. Gunn, The Ohio State University, Biomedical Research Tower, Rm. 1006, 460 W. 12th Ave., Columbus, OH 43210–1214, USA. Voice: 614-292-6036; fax: 614-292-5495. gunn.43{at}osu.edu
A key factor in the biology of Francisella spp. is lipopolysaccharide (LPS). Francisella LPS has many unique structural properties and poorly activates proinflammatory responses due to its lack of interaction with toll-like receptor 4 (TLR4). The LPS of this organism can be modified by various carbohydrates including glucose, mannose and galactosamine, which affect various aspects of virulence. Spontaneously occurring colony variants of F. tularensis have altered LPS. This altered LPS may account for the novel phenotypes of these variants that include effects on susceptibility to killing by normal human serum, intracellular survival and animal virulence. Mutants devoid of O-antigen (directed mutants in O-antigen biosynthetic genes) show reduced intracellular survival and mouse virulence. Thus, this surface component is important in F. tularensis pathogenesis, and the inability of the LPS to alarm the immune system coupled with its frequent modification/alteration likely aid the success of this pathogen during human infection.
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