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Characterization of a Pathogenic Escherichia coli Strain Derived from Oreochromis spp. Farms Using Whole-Genome Sequencing
Published on: December 23, 2022
Iron induces bimodal population development by Escherichia coli
William H DePas1, David A Hufnagel, John S Lee
1Department of Microbiology and Immunology, University of Michigan, Ann Arbor, MI 48109, USA.
Summary
Iron and superoxide stress induce rugose biofilm formation in uropathogenic Escherichia coli. This process creates distinct bacterial populations and enhances resistance to oxidative stress, offering new insights into bacterial defense mechanisms.
Area of Science:
- Microbiology
- Bacterial Pathogenesis
- Biofilm Formation
Background:
- Bacterial biofilms are complex 3D structures crucial for microbial survival and pathogenesis.
- Uropathogenic Escherichia coli (UTI89) and other enteric bacteria form biofilms that contribute to infections.
- The role of iron and oxidative stress in regulating biofilm development is not fully understood.
Purpose of the Study:
- To investigate the effect of ferric chloride on rugose biofilm formation in uropathogenic Escherichia coli UTI89 and related enteric bacteria.
- To elucidate the cellular mechanisms and stress responses involved in iron-triggered rugose biofilm development.
- To determine the impact of oxidative stress on biofilm structure and bacterial resistance.
Main Methods:
- Exposure of bacterial strains (E. coli UTI89, Citrobacter koseri, Salmonella Typhimurium) to ferric chloride.
- Analysis of gene expression (csgD, adrA, csgBAC) in different biofilm populations.
- Induction of oxidative stress using phenazine methosulfate or sodA/sodB deletion.
- Assessment of bacterial resistance to hydrogen peroxide (H2O2) toxicity.
Main Results:
- Ferric chloride exposure triggers rugose biofilm formation in UTI89, C. koseri, and S. Typhimurium.
- Two distinct cellular populations emerge: interface cells with high csgD expression and interior cells with low/undetectable matrix components.
- Superoxide generation (via phenazine methosulfate or sodA/sodB mutants) stimulates rugose biofilm formation.
- Overexpression of Mn-superoxide dismutase reduces iron-induced biofilm formation.
- Rugose biofilms exhibit increased resistance to H2O2 toxicity.
Conclusions:
- Iron and superoxide stress are key triggers for rugose biofilm formation in UTI89.
- Rugose biofilm development involves distinct bacterial subpopulations and enhanced oxidative stress resistance.
- This study reveals a novel link between iron metabolism, oxidative stress, and biofilm architecture in bacterial pathogenesis.
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