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Published on: January 27, 2021
RyhB in Avian Pathogenic Escherichia coli Regulates the Expression of Virulence-Related Genes and Contributes to
Xia Meng1,2,3, Yanfei Chen1,2,3, Peili Wang1
1Jiangsu Co-Innovation Center for the Prevention and Control of Important Animal Infectious Diseases and Zoonoses, College of Veterinary Medicine, Yangzhou University, Yangzhou 225009, China.
Abstract:
Avian pathogenic Escherichia coli (APEC) is an important member of extraintestinal pathogenic Escherichia coli (ExPEC). It shares similar pathogenic strategies with neonatal meningitis E. coli (NMEC) and may threaten human health due to its potential zoonosis. RyhB is a small non-coding RNA that regulates iron homeostasis in E. coli. However, it is unclear whether RyhB regulates meningitis occurrence. To investigate the function of RyhB in the development of meningitis, we constructed the deletion mutant APEC XM∆ryhB and the complemented mutant APEC XM∆ryhB/pryhB, established a mouse meningitis model and evaluated the role of RyhB in virulence of APEC. The results showed that the deletion of ryhB decreased biofilm formation, adhesion to the brain microvascular endothelial cell line bEnd.3 and serum resistance. RNA-seq data showed that the expression of multiple virulence-related genes changed in the ryhB deletion mutant in the presence of duck serum. Deletion of ryhB reduced the clinical symptoms of mice, such as opisthotonus, diarrhea and neurological signs, when challenged with APEC. Compared with the mice infected with the wild-type APEC, fewer histopathological lesions were observed in the brain of mice infected with the ryhB deletion mutant APEC XM∆ryhB. The bacterial loads in the tissues and the relative expression of cytokines (IL-1β, IL-6, and TNF-α) in the brain significantly decreased when challenged with the APEC XM∆ryhB. The expressions of tight junction proteins (claudin-5, occludin and ZO-1) were not reduced in the brain of mice infected with APEC XM∆ryhB; that is, the blood-brain barrier permeability of mice was not significantly damaged. In conclusion, RyhB contributes to the pathogenicity of APEC XM in the meningitis-causing process by promoting biofilm formation, adhesion to endothelial cells, serum resistance and virulence-related genes expression.
Insights
The small non-coding RNA RyhB is crucial for avian pathogenic Escherichia coli (APEC) virulence in meningitis. Deleting RyhB reduces APEC
Area of Science:
- Microbiology
- Molecular Biology
- Pathogenesis
Background:
- Avian pathogenic Escherichia coli (APEC) is an extraintestinal pathogen with zoonotic potential.
- RyhB, a small non-coding RNA, regulates iron homeostasis in E. coli.
- The role of RyhB in APEC-induced meningitis remains unexplored.
Purpose of the Study:
- To investigate the function of RyhB in the pathogenesis of APEC meningitis.
- To evaluate the impact of RyhB deletion on APEC virulence and mouse meningitis models.
Main Methods:
- Construction of APEC XM∆ryhB deletion and complemented mutants.
- Establishment of a mouse meningitis model.
- Assessment of bacterial virulence factors, gene expression (RNA-seq), and host immune responses.
Main Results:
- RyhB deletion significantly reduced APEC biofilm formation, adhesion, and serum resistance.
- Loss of RyhB attenuated clinical symptoms, bacterial load, and brain lesions in mice.
- Cytokine expression (IL-1β, IL-6, TNF-α) and tight junction protein integrity were unaffected by RyhB deletion.
Conclusions:
- RyhB is a key virulence factor for APEC meningitis.
- RyhB promotes APEC pathogenicity by enhancing biofilm formation, adhesion, serum resistance, and virulence gene expression.
