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Knockout of mlaA increases Escherichia coli virulence in a silkworm infection model
Haruka Nasu1, Riko Shirakawa1, Kazuyuki Furuta1
1Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University, Kita-ku, Okayama, Japan.
Abstract:
The mlaA gene encodes a lipoprotein to maintain an outer membrane lipid asymmetry in gram-negative bacteria. Although the role of mlaA in bacterial virulence has been studied in several bacterial species, there are no reports of its role in E. coli virulence. In this study, we found that knockout of mlaA in E. coli increased its virulence against silkworms. The mlaA-knockout mutant was sensitive to several antibiotics and detergents, but resistant to vancomycin and chlorhexidine. The mlaA-knockout mutant grew faster than the parent strain in the presence of silkworm hemolymph. The mlaA-knockout mutant also produced a larger amount of outer membrane vesicles than the parent strain. These findings suggest that mlaA knockout causes E. coli resistance to specific antimicrobial substances and increases outer membrane vesicle production, thereby enhancing E. coli virulence properties in the silkworm infection model.
Insights
Knocking out the mlaA gene in E. coli enhances its virulence in silkworms by increasing resistance to certain antimicrobials and boosting outer membrane vesicle production.
Area of Science:
- Microbiology
- Bacterial Pathogenesis
- Molecular Biology
Background:
- The mlaA gene encodes a lipoprotein crucial for maintaining outer membrane lipid asymmetry in gram-negative bacteria.
- While mlaA's role in virulence is known in other species, its function in Escherichia coli (E. coli) virulence remains uninvestigated.
Purpose of the Study:
- To investigate the role of the mlaA gene in E. coli virulence, particularly in a silkworm infection model.
- To characterize the phenotypic changes in E. coli upon mlaA gene knockout.
Main Methods:
- Construction of an mlaA knockout mutant in E. coli.
- Assessment of E. coli virulence in a silkworm model.
- Evaluation of antimicrobial sensitivity, growth in host environment, and outer membrane vesicle production.
Main Results:
- The mlaA-knockout E. coli mutant exhibited increased virulence against silkworms compared to the wild-type strain.
- The mutant showed altered sensitivity to antibiotics and detergents, being resistant to vancomycin and chlorhexidine.
- The knockout mutant displayed enhanced growth in silkworm hemolymph and produced significantly more outer membrane vesicles.
Conclusions:
- Disruption of the mlaA gene enhances E. coli virulence in silkworms.
- mlaA knockout confers resistance to specific antimicrobial agents and increases outer membrane vesicle production, contributing to increased pathogenicity.
