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Published on: February 28, 2019
A novel mouse model for septic arthritis induced by Pseudomonas aeruginosa
Tao Jin1,2, Majd Mohammad1, Zhicheng Hu1,3
1Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Göteborg, Sweden.
Abstract:
Septic arthritis is one of the most aggressive joint diseases. Although caused predominantly by S. aureus, Gram-negative bacteria, Pseudomonas aeruginosa among them, account for a significant percentage of the causal agents of septic arthritis. However, septic arthritis caused by P. aeruginosa has not been studied thus far, due to lack of an animal model. NMRI mice were inoculated with different doses of P. aeruginosa. The clinical course of septic arthritis and radiological changes of joints were examined. Furthermore, the host molecular and cellular mechanisms involved in P. aeruginosa-induced septic arthritis were investigated. Inoculation of mice with P. aeruginosa caused septic arthritis in a dose-dependent manner. Neutrophil depletion led to higher mortality and more severe joint destruction (p < 0.01). In contrast, monocyte depletion resulted in higher mortality (p < 0.05) but similar arthritis severity compared to controls. Mice depleted of CD4+ T-cells inoculated with P. aeruginosa displayed less severe bone damage (p < 0.05). For the first time, a mouse model for P. aeruginosa septic arthritis is presented. Our data demonstrate that neutrophils play a protective role in P. aeruginosa septic arthritis. Monocytes/macrophages, on the other hand, are only essential in preventing P. aeruginosa-induced mortality. Finally, CD4+ T-cells are pathogenic in P. aeruginosa septic arthritis.
Insights
A new mouse model reveals Pseudomonas aeruginosa causes septic arthritis. Neutrophils protect joints, while CD4+ T-cells worsen bone damage in this aggressive joint disease.
Area of Science:
- Infectious Diseases
- Immunology
- Orthopedics
Background:
- Septic arthritis is a severe joint disease, often caused by Staphylococcus aureus.
- Gram-negative bacteria, including Pseudomonas aeruginosa, are significant contributors to septic arthritis.
- A lack of animal models has hindered research into P. aeruginosa-induced septic arthritis.
Purpose of the Study:
- To establish and characterize a mouse model for P. aeruginosa septic arthritis.
- To investigate the host's molecular and cellular mechanisms in P. aeruginosa septic arthritis.
- To elucidate the roles of neutrophils, monocytes/macrophages, and CD4+ T-cells in the disease process.
Main Methods:
- NMRI mice were inoculated with varying doses of P. aeruginosa.
- Clinical progression and radiological joint changes were assessed.
- Cellular depletions (neutrophils, monocytes, CD4+ T-cells) were performed to evaluate their roles.
Main Results:
- P. aeruginosa inoculation induced dose-dependent septic arthritis.
- Neutrophil depletion increased mortality and joint destruction.
- Monocyte depletion raised mortality but not arthritis severity; CD4+ T-cell depletion reduced bone damage.
Conclusions:
- A novel mouse model for P. aeruginosa septic arthritis has been developed.
- Neutrophils exhibit a protective role against joint destruction in this model.
- Monocytes/macrophages are crucial for preventing mortality, while CD4+ T-cells are pathogenic.
