Reduced Virulence of an fliC Mutant of Shiga-Toxigenic Escherichia coli O113:H21

The contribution of flagellin to the virulence of the O113:H21 Shiga-toxigenic Escherichia coli (STEC) strain 98NK2 was investigated in the streptomycin-treated mouse model. Groups of mice were challenged with either the wild-type STEC or a fliC deletion derivative thereof. There was no difference i...

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Published inInfection and Immunity Vol. 74; no. 3; pp. 1962 - 1966
Main Authors Rogers, Trisha J, Paton, James C, Wang, Hui, Talbot, Ursula M, Paton, Adrienne W
Format Journal Article
LanguageEnglish
Published Washington, DC American Society for Microbiology 01.03.2006
Subjects
Animals
Bacteriology
Biological and medical sciences
Escherichia coli
Escherichia coli - genetics
Escherichia coli - immunology
Escherichia coli - pathogenicity
Escherichia coli Infections - etiology
Flagellin - genetics
Flagellin - metabolism
Fundamental and applied biological sciences. Psychology
Mice
Microbiology
Miscellaneous
Molecular Pathogenesis
Mutation
Shiga Toxins - genetics
Streptomycin - pharmacology
Virulence - genetics
Microbiology
Escherichia coli
Virulence
Bacteria
Mutation
Immunity
Enterobacteriaceae
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Abstract The contribution of flagellin to the virulence of the O113:H21 Shiga-toxigenic Escherichia coli (STEC) strain 98NK2 was investigated in the streptomycin-treated mouse model. Groups of mice were challenged with either the wild-type STEC or a fliC deletion derivative thereof. There was no difference in the level of gut colonization by the two strains, but the fliC mutant was significantly less virulent than its parent; the overall survival rates were 43.7% and 81.2%, respectively (P < 0.025). This is the first report of a nontoxic accessory virulence factor contributing to a fatal outcome of STEC infection in this model. Although H21 FliC is known to be a potent inducer of CXC chemokines, including interleukin 8, there was no obvious difference in the recruitment of polymorphonuclear leukocytes to the intestinal epithelium of mice challenged with either strain. However, immunofluorescence microscopy suggested that the fliC mutant was less capable of forming a close association with the colonic epithelium. This may have reduced the uptake of Stx2 by mice infected with the mutant.
AbstractList The contribution of flagellin to the virulence of the O113:H21 Shiga-toxigenic Escherichia coli (STEC) strain 98NK2 was investigated in the streptomycin-treated mouse model. Groups of mice were challenged with either the wild-type STEC or a fliC deletion derivative thereof. There was no difference in the level of gut colonization by the two strains, but the fliC mutant was significantly less virulent than its parent; the overall survival rates were 43.7% and 81.2%, respectively ( P < 0.025). This is the first report of a nontoxic accessory virulence factor contributing to a fatal outcome of STEC infection in this model. Although H21 FliC is known to be a potent inducer of CXC chemokines, including interleukin 8, there was no obvious difference in the recruitment of polymorphonuclear leukocytes to the intestinal epithelium of mice challenged with either strain. However, immunofluorescence microscopy suggested that the fliC mutant was less capable of forming a close association with the colonic epithelium. This may have reduced the uptake of Stx2 by mice infected with the mutant.
The contribution of flagellin to the virulence of the O113:H21 Shiga-toxigenic Escherichia coli (STEC) strain 98NK2 was investigated in the streptomycin-treated mouse model. Groups of mice were challenged with either the wild-type STEC or a fliC deletion derivative thereof. There was no difference in the level of gut colonization by the two strains, but the fliC mutant was significantly less virulent than its parent; the overall survival rates were 43.7% and 81.2%, respectively (P < 0.025). This is the first report of a nontoxic accessory virulence factor contributing to a fatal outcome of STEC infection in this model. Although H21 FliC is known to be a potent inducer of CXC chemokines, including interleukin 8, there was no obvious difference in the recruitment of polymorphonuclear leukocytes to the intestinal epithelium of mice challenged with either strain. However, immunofluorescence microscopy suggested that the fliC mutant was less capable of forming a close association with the colonic epithelium. This may have reduced the uptake of Stx2 by mice infected with the mutant.
ABSTRACT The contribution of flagellin to the virulence of the O113:H21 Shiga-toxigenic Escherichia coli (STEC) strain 98NK2 was investigated in the streptomycin-treated mouse model. Groups of mice were challenged with either the wild-type STEC or a fliC deletion derivative thereof. There was no difference in the level of gut colonization by the two strains, but the fliC mutant was significantly less virulent than its parent; the overall survival rates were 43.7% and 81.2%, respectively ( P < 0.025). This is the first report of a nontoxic accessory virulence factor contributing to a fatal outcome of STEC infection in this model. Although H21 FliC is known to be a potent inducer of CXC chemokines, including interleukin 8, there was no obvious difference in the recruitment of polymorphonuclear leukocytes to the intestinal epithelium of mice challenged with either strain. However, immunofluorescence microscopy suggested that the fliC mutant was less capable of forming a close association with the colonic epithelium. This may have reduced the uptake of Stx2 by mice infected with the mutant.
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Author Rogers, Trisha J
Paton, Adrienne W
Talbot, Ursula M
Wang, Hui
Paton, James C
AuthorAffiliation School of Molecular and Biomedical Science, University of Adelaide, Adelaide, S.A. 5005, Australia
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Editor: A. D. O'Brien
Corresponding author. Mailing address: School of Molecular and Biomedical Science, University of Adelaide, Adelaide, S.A. 5005, Australia. Phone: 61-8-83037552. Fax: 61-8-83033262. E-mail: adrienne.paton@adelaide.edu.au.
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Snippet The contribution of flagellin to the virulence of the O113:H21 Shiga-toxigenic Escherichia coli (STEC) strain 98NK2 was investigated in the...
Classifications Services IAI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit...
ABSTRACT The contribution of flagellin to the virulence of the O113:H21 Shiga-toxigenic Escherichia coli (STEC) strain 98NK2 was investigated in the...
The contribution of flagellin to the virulence of the O113:H21 Shiga-toxigenic Escherichia coli (STEC) strain 98NK2 was investigated in the...
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StartPage 1962
SubjectTerms Animals
Bacteriology
Biological and medical sciences
Escherichia coli
Escherichia coli - genetics
Escherichia coli - immunology
Escherichia coli - pathogenicity
Escherichia coli Infections - etiology
Flagellin - genetics
Flagellin - metabolism
Fundamental and applied biological sciences. Psychology
Mice
Microbiology
Miscellaneous
Molecular Pathogenesis
Mutation
Shiga Toxins - genetics
Streptomycin - pharmacology
Virulence - genetics
Title Reduced Virulence of an fliC Mutant of Shiga-Toxigenic Escherichia coli O113:H21
URI http://iai.asm.org/content/74/3/1962.abstract
https://www.ncbi.nlm.nih.gov/pubmed/16495575
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