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IbeR facilitates stress-resistance, invasion and pathogenicity of avian pathogenic Escherichia coli.

Wang S, Bao Y, Meng Q, Xia Y, Zhao Y, Wang Y, Tang F, ZhuGe X, Yu S, Han X, Dai J, Lu C - PLoS ONE (2015)

Bottom Line: Inactivation of ibeR led to attenuated virulence and reduced invasion capacity towards DF-1 cells, brains and cerebrospinal fluid (CSF) in vitro and in vivo.These virulence-related phenotypes were restored by genetic complementation.Quantitative real-time reverse transcription PCR revealed that IbeR controlled expression of stress-resistance genes and virulence genes, which might led to the associated virulence phenotype.

View Article: PubMed Central - PubMed

Affiliation: Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Shanghai, 200241, China; Key Lab of Animal Bacteriology, Ministry of Agriculture, Nanjing Agricultural University, Nanjing, 210095, China.

ABSTRACT
Systemic infections by avian pathogenic Escherichia coli (APEC) are economically devastating to poultry industries worldwide. IbeR, located on genomic island GimA, was shown to serve as an RpoS-like regulator in rpoS gene mutation neonatal meningitis E. coli (NMEC) RS218. However, the role of IbeR in pathogenicity of APEC carrying active RpoS has not yet been investigated. We showed that the APEC IbeR could elicit antibodies in infected ducks, suggesting that IbeR might be involved in APEC pathogenicity. To investigate the function of IbeR in APEC pathogenesis, mutant and complementation strains were constructed and characterized. Inactivation of ibeR led to attenuated virulence and reduced invasion capacity towards DF-1 cells, brains and cerebrospinal fluid (CSF) in vitro and in vivo. Bactericidal assays demonstrated that the mutant strain had impaired resistance to environmental stress and specific pathogen-free (SPF) chicken serum. These virulence-related phenotypes were restored by genetic complementation. Quantitative real-time reverse transcription PCR revealed that IbeR controlled expression of stress-resistance genes and virulence genes, which might led to the associated virulence phenotype.

No MeSH data available.


Related in: MedlinePlus

Quantification of gene expression.Expression of genes involved in resistance and virulence were measured by qRT-PCR for each strain. Data were normalized to the housekeeping gene dnaE. Results are relative expression ratios compared to wild-type strain DE205B. *** p < 0.001; **p < 0.01; *p < 0.05. The error bars indicate standard deviations.
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pone.0119698.g006: Quantification of gene expression.Expression of genes involved in resistance and virulence were measured by qRT-PCR for each strain. Data were normalized to the housekeeping gene dnaE. Results are relative expression ratios compared to wild-type strain DE205B. *** p < 0.001; **p < 0.01; *p < 0.05. The error bars indicate standard deviations.

Mentions: To identify metabolic defaults that was responsible for the decreased resistance and attenuated virulence, the expression levels of range of genes involved in resistance and virulence were analyzed by qRT-PCR for various strains. The results showed that the expression of lpdA, tufB, gapA, aphC, ibeA, ibeB and fimC were significantly upregulated in the mutant strain ΔibeR. The mRNA levels were moderately decreased in the mutant strain ΔibeR by 0.23 for ompA, 0.26 for aatA, 0.56 for iucD and 0.26 for luxS genes (p < 0.01). However, the expression of genes involved in oxidative stress response katE, sodC, osmC were significantly reduced in the mutant strain ΔibeR (Fig. 6).


IbeR facilitates stress-resistance, invasion and pathogenicity of avian pathogenic Escherichia coli.

Wang S, Bao Y, Meng Q, Xia Y, Zhao Y, Wang Y, Tang F, ZhuGe X, Yu S, Han X, Dai J, Lu C - PLoS ONE (2015)

Quantification of gene expression.Expression of genes involved in resistance and virulence were measured by qRT-PCR for each strain. Data were normalized to the housekeeping gene dnaE. Results are relative expression ratios compared to wild-type strain DE205B. *** p < 0.001; **p < 0.01; *p < 0.05. The error bars indicate standard deviations.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4359115&req=5

pone.0119698.g006: Quantification of gene expression.Expression of genes involved in resistance and virulence were measured by qRT-PCR for each strain. Data were normalized to the housekeeping gene dnaE. Results are relative expression ratios compared to wild-type strain DE205B. *** p < 0.001; **p < 0.01; *p < 0.05. The error bars indicate standard deviations.
Mentions: To identify metabolic defaults that was responsible for the decreased resistance and attenuated virulence, the expression levels of range of genes involved in resistance and virulence were analyzed by qRT-PCR for various strains. The results showed that the expression of lpdA, tufB, gapA, aphC, ibeA, ibeB and fimC were significantly upregulated in the mutant strain ΔibeR. The mRNA levels were moderately decreased in the mutant strain ΔibeR by 0.23 for ompA, 0.26 for aatA, 0.56 for iucD and 0.26 for luxS genes (p < 0.01). However, the expression of genes involved in oxidative stress response katE, sodC, osmC were significantly reduced in the mutant strain ΔibeR (Fig. 6).

Bottom Line: Inactivation of ibeR led to attenuated virulence and reduced invasion capacity towards DF-1 cells, brains and cerebrospinal fluid (CSF) in vitro and in vivo.These virulence-related phenotypes were restored by genetic complementation.Quantitative real-time reverse transcription PCR revealed that IbeR controlled expression of stress-resistance genes and virulence genes, which might led to the associated virulence phenotype.

View Article: PubMed Central - PubMed

Affiliation: Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Shanghai, 200241, China; Key Lab of Animal Bacteriology, Ministry of Agriculture, Nanjing Agricultural University, Nanjing, 210095, China.

ABSTRACT
Systemic infections by avian pathogenic Escherichia coli (APEC) are economically devastating to poultry industries worldwide. IbeR, located on genomic island GimA, was shown to serve as an RpoS-like regulator in rpoS gene mutation neonatal meningitis E. coli (NMEC) RS218. However, the role of IbeR in pathogenicity of APEC carrying active RpoS has not yet been investigated. We showed that the APEC IbeR could elicit antibodies in infected ducks, suggesting that IbeR might be involved in APEC pathogenicity. To investigate the function of IbeR in APEC pathogenesis, mutant and complementation strains were constructed and characterized. Inactivation of ibeR led to attenuated virulence and reduced invasion capacity towards DF-1 cells, brains and cerebrospinal fluid (CSF) in vitro and in vivo. Bactericidal assays demonstrated that the mutant strain had impaired resistance to environmental stress and specific pathogen-free (SPF) chicken serum. These virulence-related phenotypes were restored by genetic complementation. Quantitative real-time reverse transcription PCR revealed that IbeR controlled expression of stress-resistance genes and virulence genes, which might led to the associated virulence phenotype.

No MeSH data available.


Related in: MedlinePlus