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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

Determination of bacterial virulence.Seven-day-old ducks were inoculated intratracheally with DE205B, ΔibeR, CΔibeR or ΔibeRibeA at 107 colony-forming units (CFUs). Negative controls were injected with PBS. Survival was monitored until 7 days post infection.
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pone.0119698.g003: Determination of bacterial virulence.Seven-day-old ducks were inoculated intratracheally with DE205B, ΔibeR, CΔibeR or ΔibeRibeA at 107 colony-forming units (CFUs). Negative controls were injected with PBS. Survival was monitored until 7 days post infection.

Mentions: To investigate whether IbeR was involved in bacterial virulence, groups of 10 ducks were infected with 1 × 107 CFU of wild-type, mutant, or complementation strains. Mortality was observed for 7 days post challenge. As shown in Fig. 3, the mortality of DE205B, ΔibeR, CΔibeR and ΔibeRibeA were 90%(9/10), 20%(2/10), 70%(7/10) and 10%(1/10), respectively. These results indicated that loss of IbeR or IbeR-IbeA led to attenuation of virulence in birds. Virulence was restored in the complementation strain.


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)

Determination of bacterial virulence.Seven-day-old ducks were inoculated intratracheally with DE205B, ΔibeR, CΔibeR or ΔibeRibeA at 107 colony-forming units (CFUs). Negative controls were injected with PBS. Survival was monitored until 7 days post infection.
© Copyright Policy
Related In: Results  -  Collection

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

pone.0119698.g003: Determination of bacterial virulence.Seven-day-old ducks were inoculated intratracheally with DE205B, ΔibeR, CΔibeR or ΔibeRibeA at 107 colony-forming units (CFUs). Negative controls were injected with PBS. Survival was monitored until 7 days post infection.
Mentions: To investigate whether IbeR was involved in bacterial virulence, groups of 10 ducks were infected with 1 × 107 CFU of wild-type, mutant, or complementation strains. Mortality was observed for 7 days post challenge. As shown in Fig. 3, the mortality of DE205B, ΔibeR, CΔibeR and ΔibeRibeA were 90%(9/10), 20%(2/10), 70%(7/10) and 10%(1/10), respectively. These results indicated that loss of IbeR or IbeR-IbeA led to attenuation of virulence in birds. Virulence was restored in the complementation strain.

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