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Role of outer membrane protein T in pathogenicity of avian pathogenic Escherichia coli

Hassan M A Hejair1, Jiale Ma2, Yingchu Zhu2

  • 1College of Veterinary Medicine, Nanjing Agricultural University, Key Lab of Animal Bacteriology, Ministry of Agriculture, Nanjing 210095, China; College of Veterinary Sciences, University of Nyala, Nyala, Sudan.

Research in Veterinary Science
|February 16, 2017
PubMed

Insights

Outer membrane protein T (OmpT) is crucial for avian pathogenic E. coli (APEC) virulence. Deleting the ompT gene significantly reduced APEC

Area of Science:

  • Microbiology
  • Pathogenesis
  • Molecular Biology

Background:

  • Neonatal meningitis Escherichia coli (NMEC) pathogenesis involves outer membrane protein T (OmpT).
  • The role of OmpT in avian pathogenic E. coli (APEC) remains uncharacterized.

Purpose of the Study:

  • To investigate the role of OmpT in APEC pathogenesis.
  • To evaluate the impact of ompT gene deletion on APEC virulence and colonization.

Main Methods:

  • Construction and characterization of an ompT-deleted APEC mutant strain (ΔOmpT).
  • Assessment of bacterial adherence and invasion capabilities using mouse brain microvascular endothelial cells (BMEC).
  • Determination of 50% lethal dose (LD50) in duckling and mouse models.
  • Evaluation of bacterial colonization and invasion in host tissues (brains, lungs, blood).
  • Quantitative real-time reverse transcription-PCR (qRT-PCR) to analyze gene expression levels.

Main Results:

  • OmpT inactivation significantly reduced APEC adherence (43.8%) and invasion (28.8%) to BMEC cells.
  • Deletion of ompT increased bacterial virulence in ducklings (15.2-fold) and mice (9.7-fold) based on LD50.
  • Loss of OmpT decreased APEC colonization and invasion in brains (2-fold), lungs (1.96-fold), and blood (1.7-fold).
  • These virulence defects were partially restored by genetic complementation.
  • Quantitative real-time reverse transcription-PCR revealed decreased expression of ompA, fimC, and tsh in the ΔOmpT mutant.

Conclusions:

  • Inactivation of the ompT gene significantly attenuates APEC virulence.
  • OmpT contributes to APEC's adhesion, invasion, and colonization capabilities.
  • Reduced expression of ompA, fimC, and tsh may mediate the attenuated virulence observed in the ΔOmpT mutant.
  • OmpT is implicated as a significant factor in APEC pathogenicity.
Keywords:
APECAdhesionInvasionPathogenicityompT

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