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05:31
Purification and Visualization of Lipopolysaccharide from Gram-negative Bacteria by Hot Aqueous-phenol Extraction
Published on: May 28, 2012
The structure and function of Francisella lipopolysaccharide
1The Center for Microbial Interface Biology, The Ohio State University, Biomedical Research Tower, Rm. 1006, 460 W. 12th Ave., Columbus, OH 43210-1214, USA. gunn.43@osu.edu
Annals of the New York Academy of Sciences
|March 31, 2007
Summary
Francisella lipopolysaccharide (LPS) poorly activates immune responses and can be modified, aiding bacterial virulence. Altered LPS in variants impacts serum resistance, intracellular survival, and animal virulence, highlighting its role in pathogenesis.
Area of Science:
- Microbiology
- Immunology
- Pathogenesis
Background:
- Lipopolysaccharide (LPS) is crucial for Francisella spp. biology.
- Francisella LPS exhibits unique structures and weak interaction with toll-like receptor 4 (TLR4), resulting in limited proinflammatory responses.
- LPS modifications by carbohydrates like glucose, mannose, and galactosamine influence virulence.
Purpose of the Study:
- To investigate the role of lipopolysaccharide (LPS) structure and modification in Francisella tularensis pathogenesis.
- To understand how altered LPS affects bacterial phenotypes, including serum resistance, intracellular survival, and virulence.
- To elucidate the contribution of LPS to the success of Francisella during human infection.
Main Methods:
- Analysis of spontaneously occurring colony variants of F. tularensis with altered LPS.
- Generation and characterization of directed mutants lacking O-antigen.
- Assessment of bacterial phenotypes including susceptibility to serum killing, intracellular survival, and animal virulence.
Main Results:
- Spontaneous LPS alterations in F. tularensis variants correlate with changes in serum resistance, intracellular survival, and animal virulence.
- Mutants lacking O-antigen display reduced intracellular survival and mouse virulence.
- The unique LPS structure and its modifications contribute to F. tularensis pathogenesis.
Conclusions:
- Francisella LPS plays a significant role in F. tularensis pathogenesis.
- The LPS's limited immune activation and frequent modifications are key strategies for Francisella survival during infection.
- Targeting LPS structure or modification could be a potential therapeutic strategy against Francisella infections.
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