Abstract

Escherichia coli is a versatile bacterial species that includes both harmless commensal strains and pathogenic strains found in the gastrointestinal tract in humans and warm-blooded animals. The growing amount of DNA sequence information generated in the era of “genomics” has helped to increase our understanding of the factors and mechanisms involved in the diversification of this bacterial species. The pathogenic side of E. coli that is afforded through horizontal transfers of genes encoding virulence factors enables this bacterium to become a highly diverse and adapted pathogen that is responsible for intestinal or extraintestinal diseases in humans and animals. Many of the accessory genes acquired by horizontal transfers form syntenic blocks and are recognized as genomic islands (GIs). These genomic regions contribute to the rapid evolution, diversification and adaptation of E. coli variants because they are frequently subject to rearrangements, excision and transfer, as well as to further acquisition of additional DNA. Here, we review a subgroup of GIs from E. coli termed pathogenicity islands (PAIs), a concept defined in the late 1980s by Jörg Hacker and colleagues in Werner Goebel’s group at the University of Würzburg, Würzburg, Germany. As with other GIs, the PAIs comprise large genomic regions that differ from the rest of the genome by their G + C content, by their typical insertion within transfer RNA genes, and by their harboring of direct repeats (at their ends), integrase determinants, or other mobility loci. The hallmark of PAIs is their contribution to the emergence of virulent bacteria and to the development of intestinal and extraintestinal diseases. This review summarizes the current knowledge on the structure and functional features of PAIs, on PAI-encoded E. coli pathogenicity factors and on the role of PAIs in host–pathogen interactions.

Highlights

  • Escherichia coli is a versatile bacterial species that has an extensive phylogenetic substructure comprising eight phylogroups (A, B1, B2, C, D, E, F, and G) that are roughly linked to the lifestyles of the different strains (Milkman, 1973; Selander et al, 1987; Escobar-Páramo et al, 2004a; Clermont et al, 2019)

  • The detection methods usually use the following indicative features of the horizontal origin of genomic islands (GI) and pathogenicity islands (PAI): (i) biased sequence composition, (ii) gene or motif content, and (iii) sporadic phylogenetic distribution assessed by the identification of regions only present in a subset of genomes and/or containing genes usually found in PAIs, such as virulence genes, transposase, integrases or genes coding unknown functions (Langille et al, 2010; Lu and Leong, 2016; Bertelli et al, 2019)

  • PAIs are widespread in E. coli and are major actors in the genome plasticity of this bacterium

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Summary

INTRODUCTION

Escherichia coli is a versatile bacterial species that has an extensive phylogenetic substructure comprising eight phylogroups (A, B1, B2, C, D, E, F, and G) that are roughly linked to the lifestyles of the different strains (Milkman, 1973; Selander et al, 1987; Escobar-Páramo et al, 2004a; Clermont et al, 2019). PAIs in E. coli and coexist in good health with the host, with strains providing mutual benefits for decades These commensal strains rarely cause diseases in healthy hosts, as they lack specialized virulence traits; they typically originate from phylogroup A (Herzer et al, 1990; Escobar-Páramo et al, 2004b). Group B2 has the greatest diversity among all E. coli phylogroups (Touchon et al, 2009), suggesting that it has subspecies status and includes subgroups correlated with a flexible gene pool (Le Gall et al, 2007; Lescat et al, 2009) This flexible gene pool comprises genes for various combinations of virulence factors, such as adhesins, iron-acquisition systems, host defense-avoidance mechanisms and toxins (Croxen and Finlay, 2010). This review summarizes the current knowledge on the structure and functional features of PAIs, on E. coli PAI-encoded pathogenicity factors and on the role of PAIs in host-pathogen interactions

STRUCTURAL FEATURES OF PATHOGENICITY ISLANDS
INSTABILITY AND MOTILIY OF PATHOGENICITY ISLANDS
Physiopathology of ExPEC and AIEC Infections
PAIs in ExPEC and AIEC
Meningitis associated and temperature regulated fimbriae
Autotransporter adhesin
Cytotoxic metalloprotease exihiting mucinase and proinflammatory activity
PATHOTYPE UPEC
Resistance to protamine and urine survival
Chromosomal insertion site
Sit system Yersiniabactin
DIARRHEAGENIC ESCHERICHIA coli
Physiopathology of DEC
PAI espC PAI sit HPI
CONCLUSION
Findings
AUTHOR CONTRIBUTIONS

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