ArticlePLoS pathogens2013
The genetic basis of Escherichia coli pathoadaptation to macrophages.
Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed.
- Simulating the host niche: balancing complexity and control in the experimental evolution of antibiotic resistance and pathoadaptation.Microbiology (Reading, England) · 2026Review
- Beyond Resistance: Phenotypic Plasticity in Bacterial Responses to Antibiotics, Oxidative Stress and Antimicrobial Photodynamic Inactivation.Molecules (Basel, Switzerland) · 2026Review
- Parallel within-host evolution alters virulence factors in an opportunistic Klebsiella pneumoniae during a hospital outbreak.Nature communications · 2025Article
- A survey of computational approaches for characterizing microbial interactions in microbial mats.Genome biology · 2025Review
- Type 1 fimbrial phase variation in multidrug-resistant asymptomatic uropathogenic Escherichia coli clinical isolates upon adherence to HTB-4 cells.Folia microbiologica · 2024Article
- Experimental evolution ofmBio · 2024Article
- Bacterial capsules: Occurrence, mechanism, and function.NPJ biofilms and microbiomes · 2024Review
- Genetically Engineered Microorganisms and Their Impact on Human Health.International journal of clinical practice · 2024Review
- Intrahost evolution of the gut microbiota.Nature reviews. Microbiology · 2023Review
- Targeted IS-element sequencing uncovers transposition dynamics during selective pressure in enterococci.PLoS pathogens · 2023Article
- Intracellular Experimental Evolution ofACS infectious diseases · 2023Article
- Interactions between host epithelial cells andEmerging microbes & infections · 2022Article
- IgaA Protein, GumB, Has a Global Impact on the Transcriptome and Surface Proteome of Serratia marcescens.Infection and immunity · 2022Article
- Adaptation to novel spatially-structured environments is driven by the capsule and alters virulence-associated traits.Nature communications · 2022Article
- Genetically stable CRISPR-based kill switches for engineered microbes.Nature communications · 2022Article
- Predatory Bacteria Select for Sustained Prey Diversity.Microorganisms · 2021Article
- Functional genomics study of Pseudomonas putida to determine traits associated with avoidance of a myxobacterial predator.Scientific reports · 2021Article
- The Rcs Stress Response System Regulator GumB Modulates Serratia marcescens-Induced Inflammation and Bacterial Proliferation in a Rabbit Keratitis Model and CytotoxicityInfection and immunity · 2021Article
- Long COVID or Post-acute Sequelae of COVID-19 (PASC): An Overview of Biological Factors That May Contribute to Persistent Symptoms.Frontiers in microbiology · 2021Review
- A Longitudinal Evaluation of the Bacterial Pathogens Colonizing Chronic Non-Healing Wound Sites at a United States Military Treatment Facility in the Pacific Region.Infection and drug resistance · 2021Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antagonistic interactions are likely important driving forces of the evolutionary process underlying bacterial genome complexity and diversity. We hypothesized that the ability of evolved bacteria to escape specific components of host innate immunity, such as phagocytosis and killing by macrophages (MΦ), is a critical trait relevant in the acquisition of bacterial virulence. Here, we used a combination of experimental evolution, phenotypic characterization, genome sequencing and mathematical modeling to address how fast, and through how many adaptive steps, a commensal Escherichia coli (E. coli) acquire this virulence trait. We show that when maintained in vitro under the selective pressure of host MΦ commensal E. coli can evolve, in less than 500 generations, virulent clones that escape phagocytosis and MΦ killing in vitro, while increasing their pathogenicity in vivo, as assessed in mice. This pathoadaptive process is driven by a mechanism involving the insertion of a single transposable element into the promoter region of the E. coli yrfF gene. Moreover, transposition of the IS186 element into the promoter of Lon gene, encoding an ATP-dependent serine protease, is likely to accelerate this pathoadaptive process. Competition between clones carrying distinct beneficial mutations dominates the dynamics of the pathoadaptive process, as suggested from a mathematical model, which reproduces the observed experimental dynamics of E. coli evolution towards virulence. In conclusion, we reveal a molecular mechanism explaining how a specific component of host innate immunity can modulate microbial evolution towards pathogenicity.
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