Limits...
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

IbeR was involved in invasion DF-1 cells by DE205B.Invasion assays were performed on DF-1 cells. Values are average of three independent experiments. The error bars indicate standard deviations. One-way ANOVA was performed for statistical significance analysis. *** p < 0.001; ** p < 0.01; * p < 0.05.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4359115&req=5

pone.0119698.g004: IbeR was involved in invasion DF-1 cells by DE205B.Invasion assays were performed on DF-1 cells. Values are average of three independent experiments. The error bars indicate standard deviations. One-way ANOVA was performed for statistical significance analysis. *** p < 0.001; ** p < 0.01; * p < 0.05.

Mentions: The role of IbeR in adhesion and invasion of APEC to avian cell lines was determined. The adhesion capacity of mutant strain ΔibeR was similar to the wild-type strain DE205B and the complementation strain CΔibeR, indicating that IbeR did not affect APEC adhesion of DF-1 cells (data not shown). A significant reduction of 35% was detected in invasion of the mutant strain ΔibeR compared with DE205B (p < 0.01) (Fig. 4). Invasion capacity was restored in complementation strain CΔibeR, with a significant difference compared to strains ΔibeR (p < 0.05). Similar to the results of the virulence test, the double-mutant strain ΔibeRibeA showed decreased ability to invade host cells compared to wild-type and single mutant strains (Fig. 4). Thus, we assumed that IbeR was involved in the invasion of APEC into DF-1 cells.


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)

IbeR was involved in invasion DF-1 cells by DE205B.Invasion assays were performed on DF-1 cells. Values are average of three independent experiments. The error bars indicate standard deviations. One-way ANOVA was performed for statistical significance analysis. *** p < 0.001; ** p < 0.01; * p < 0.05.
© Copyright Policy
Related In: Results  -  Collection

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

pone.0119698.g004: IbeR was involved in invasion DF-1 cells by DE205B.Invasion assays were performed on DF-1 cells. Values are average of three independent experiments. The error bars indicate standard deviations. One-way ANOVA was performed for statistical significance analysis. *** p < 0.001; ** p < 0.01; * p < 0.05.
Mentions: The role of IbeR in adhesion and invasion of APEC to avian cell lines was determined. The adhesion capacity of mutant strain ΔibeR was similar to the wild-type strain DE205B and the complementation strain CΔibeR, indicating that IbeR did not affect APEC adhesion of DF-1 cells (data not shown). A significant reduction of 35% was detected in invasion of the mutant strain ΔibeR compared with DE205B (p < 0.01) (Fig. 4). Invasion capacity was restored in complementation strain CΔibeR, with a significant difference compared to strains ΔibeR (p < 0.05). Similar to the results of the virulence test, the double-mutant strain ΔibeRibeA showed decreased ability to invade host cells compared to wild-type and single mutant strains (Fig. 4). Thus, we assumed that IbeR was involved in the invasion of APEC into DF-1 cells.

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