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Published on: January 2, 2015
Conflicting roles for a cell surface modification in Salmonella.
John F May1, Eduardo A Groisman
1Department of Microbial Pathogenesis, Yale School of Medicine, New Haven, CT 06536, USA.
Salmonella regulates lipopolysaccharide (LPS) O-antigen length to adapt to bile. Long O-antigen chains impair growth in bile, especially with enterobacterial common antigen, suggesting condition-specific adaptation.
Area of Science:
- Microbiology
- Bacterial Pathogenesis
- Molecular Biology
Background:
- Chemical modifications of bacterial cell envelopes can increase resistance to antimicrobials.
- The regulation of these modifications under specific conditions is not fully understood.
- Lipopolysaccharide (LPS) O-antigen length is a key variable in the Gram-negative bacterial outer membrane.
Purpose of the Study:
- To investigate the role of regulated O-antigen length variations in lipopolysaccharide (LPS).
- To understand why LPS modifications occur only under specific conditions in Salmonella.
- To examine the impact of O-antigen length on Salmonella growth in bile.
Main Methods:
- Examined the PmrA/PmrB two-component system, a major regulator of LPS alterations in Salmonella.
- Assessed the growth of Salmonella in bile under conditions affecting O-antigen length.
- Investigated the role of specific genes (wzz(st), wzz(fepE)) and other LPS modifications.
Main Results:
- Activation of the PmrA/PmrB system impaired Salmonella growth in bile.
- This growth defect was dependent on the wzz(st) gene, which mediates long O-antigen production.
- Long O-antigen inhibited bile growth only when enterobacterial common antigen was present.
Conclusions:
- Salmonella regulates O-antigen length to adapt to environmental conditions, such as the presence of bile.
- The interplay between O-antigen length and enterobacterial common antigen influences bile resistance.
- These findings highlight a mechanism for Salmonella to modulate its cell envelope for survival during infection.
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