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.
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http://dx.doi.org/10.1128/IAI.00241-18 | DOI Listing |
Infect Immun
August 2018
Departamento de Biofísica, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil
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.
View Article and Find Full Text PDFPLoS One
April 2013
Departamento de Biofísica, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brasil.
The purpose of this study was to compare histopathological changes in the lungs of chickens infected with avian pathogenic (APEC) and avian fecal (A(fecal)) Escherichia coli strains, and to analyze how the interaction of the bacteria with avian macrophages relates to the outcome of the infection. Chickens were infected intratracheally with three APEC strains, MT78, IMT5155, and UEL17, and one non-pathogenic A(fecal) strain, IMT5104. The pathogenicity of the strains was assessed by isolating bacteria from lungs, kidneys, and spleens at 24 h post-infection (p.
View Article and Find Full Text PDFVet Microbiol
February 2011
Departamento de Biofísica, Universidade Federal do Rio Grande do Sul, PO Box 15005, 9500 Av. Bento Gonçalves, 91501-970 Porto Alegre, RS, Brazil.
Avian pathogenic Escherichia coli (APEC) are responsible for extraintestinal diseases, called colibacillosis, in avian species. The most severe manifestation of the disease is colisepticemia that usually starts at the respiratory tract and may result in bird death. However, it is not yet clear how APEC cross the respiratory epithelium and get into the bloodstream.
View Article and Find Full Text PDFInfect Immun
January 2003
Département de Pathologie et Microbiologie, Faculté de Médecine Vétérinaire, Université de Montréal, St. Hyacinthe, Québec J2S 7C6, Canada.
In chickens, colibacillosis is caused by avian pathogenic Escherichia coli (APEC) via respiratory tract infection. Many virulence factors, including type 1 (F1A) and P (F11) fimbriae, curli, aerobactin, K1 capsule, and temperature-sensitive hemagglutinin (Tsh) and plasmid DNA regions have been associated with APEC. A strong correlation between serum resistance and virulence has been demonstrated, but roles of virulence factors in serum resistance have not been well elucidated.
View Article and Find Full Text PDFAvian Dis
December 2000
Station de Pathologie aviaire et de Parasitologie, INRA, Nouzilly, France.
Several studies suggest that the expression of F1 fimbriae could be involved in the virulence of Escherichia coli for chickens. F1 fimbriae display multivalent properties such as adhesion to epithelia or interaction with the immune system that imply specific interactions between the adhesin FimH and different cell receptors. We constructed a delta fimH mutant of the avian pathogenic E.
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