The Periplasmic Trehalase Affects Type 1 Fimbria Production and Virulence of Extraintestinal Pathogenic Escherichia coli Strain MT78

Extraintestinal pathogenic (ExPEC) is responsible for various infections outside the gastrointestinal tract in humans and other animals. ExPEC strain MT78 is invasive to various nonphagocytic cells and highly virulent To identify genes required for invasion of nonphagocytic cells by this strain, we...

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Veröffentlicht in:Infection and immunity 2018-08, Vol.86 (8)
Hauptverfasser: Pavanelo, Daniel Brisotto, Houle, Sébastien, Matter, Letícia Beatriz, Dozois, Charles Martin, Horn, Fabiana
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Sprache:eng
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Zusammenfassung:Extraintestinal pathogenic (ExPEC) is responsible for various infections outside the gastrointestinal tract in humans and other animals. ExPEC strain MT78 is invasive to various nonphagocytic cells and highly virulent To identify genes required for invasion of nonphagocytic cells by this strain, we applied signature-tagged mutagenesis to generate a library of mutants and tested them for invasion of avian fibroblasts. Mutants showing reduced cellular invasion included those with insertions in the operon, encoding type 1 fimbriae. Another attenuated mutant showed a disruption in the gene, which encodes a periplasmic trehalase. The substrate of TreA, trehalose, can be metabolized and used as a carbon source or can serve as an osmoprotectant under conditions of osmotic stress in K-12. We generated and characterized mutant MT78Δ In contrast to the wild type, MT78Δ was able to grow under osmotic stress caused by 0.6 M urea but not in minimal M9 medium with trehalose as the only carbon source. It presented decreased association and invasion of avian fibroblasts, decreased yeast agglutination titer, and impaired type 1 fimbria production. In a murine model of urinary tract infection, MT78Δ was less able to colonize the bladder. All phenotypes were rescued in the complemented mutant. Our results show that the gene is needed for optimal production of type 1 fimbriae in ExPEC strain MT78 and that loss of significantly reduces its cell invasion capacity and colonization of the bladder in a murine model of urinary tract infection.
ISSN:0019-9567
1098-5522
DOI:10.1128/IAI.00241-18