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Long Term Chronic Pseudomonas aeruginosa Airway Infection in Mice
Published on: March 17, 2014
DeaD contributes to Pseudomonas aeruginosa virulence in a mouse acute pneumonia model
Hao Tan1, Lu Zhang1, Qiang Zhao2
1State Key Laboratory of Medicinal Chemical Biology, Key Laboratory of Molecular Microbiology and Technology of the Ministry of Education, Department of Microbiology, College of Life Sciences, Nankai University, Tianjin 300071, China.
Abstract:
DExD/H box RNA helicases play essential roles in various biological processes in prokaryotes and eukaryotes. By screening Pseudomonas aeruginosa strains with mutations in various DExD/H box helicase genes, we identified that deaD was required for bacterial cytotoxicity and virulence in a mouse acute pneumonia model. Compared to a wild-type strain and its complementation strain, the deaD mutant induced less production of proinflammatory cytokines, neutrophil infiltration and lung damage during infection. We further found that the RNA helicase activity of DeaD was required for the expression of type III secretion system (T3SS) genes. Overexpression of ExsA, a master activator of the T3SS, restored the expression of T3SS genes as well as the virulence of the deaD mutant, suggesting that the attenuated virulence of the deaD mutant was mainly due to the defective T3SS. Overall, our results reveal a role of DeaD in the virulence of P. aeruginosa.
Insights
The DeaD protein is crucial for Pseudomonas aeruginosa virulence. Its absence reduces bacterial cytotoxicity and lung damage by affecting the type III secretion system (T3SS).
Area of Science:
- Microbiology
- Molecular Biology
- Pathogenesis
Background:
- DExD/H box RNA helicases are vital for numerous cellular processes in all domains of life.
- Pseudomonas aeruginosa is an opportunistic pathogen causing severe infections, including pneumonia.
Purpose of the Study:
- To investigate the role of DExD/H box helicase genes in Pseudomonas aeruginosa virulence.
- To elucidate the specific function of the DeaD helicase in bacterial pathogenesis.
Main Methods:
- Screening of Pseudomonas aeruginosa strains with mutations in DExD/H box helicase genes.
- Evaluation of bacterial cytotoxicity and virulence in a mouse acute pneumonia model.
- Analysis of proinflammatory cytokine production, neutrophil infiltration, and lung damage.
- Assessment of type III secretion system (T3SS) gene expression and the role of ExsA.
Main Results:
- The deaD mutant exhibited significantly reduced bacterial cytotoxicity and virulence in a mouse model.
- The deaD mutant induced lower levels of proinflammatory cytokines, neutrophil infiltration, and lung damage.
- DeaD's RNA helicase activity was essential for the expression of type III secretion system (T3SS) genes.
- Overexpression of ExsA, a T3SS activator, restored T3SS gene expression and virulence in the deaD mutant.
Conclusions:
- DeaD is a key factor in Pseudomonas aeruginosa virulence.
- The attenuated virulence of the deaD mutant is primarily attributed to the defective type III secretion system (T3SS).
- DeaD's RNA helicase activity is essential for regulating T3SS gene expression and bacterial pathogenesis.
