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Profiling of cellular immune responses to Mycoplasma pulmonis infection in C57BL/6 and DBA/2 mice
Tussapon Boonyarattanasoonthorn1, Yaser Hosny Ali Elewa2, Hassan T Tag-El-Din-Hassan3
1Laboratory of Laboratory Animal Science and Medicine, Department of Applied Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo 060-0818, Japan.
Abstract:
Mycoplasma infections cause respiratory tract damages and atypical pneumonia, resulting in serious problems in humans and animals worldwide. It is well known that laboratory inbred mouse strains show various susceptibility to Mycoplasma pulmonis (M. pulmonis) infection, which causes murine respiratory mycoplasmosis. In this study, we aimed to demonstrate the difference in cellular immune responses between resistant strain, C57BL/6NCrSlc (B6) and susceptible strain, DBA/2CrSlc (D2) after challenging M. pulmonis infection. D2 mice showed higher amount of bacterial proliferation in lung, higher pulmonary infiltration of immune cells such as neutrophils, macrophages, and lymphocytes, and higher levels of interleukin (IL)-1β, IL-6, IL-17A, and tumor necrosis factor-α in bronchoalveolar lavage fluid than did B6 mice. The results of this study suggest that D2 mice are more susceptible than B6 mice to M. pulmonis infection due to a hyper-immune inflammatory response.
Insights
DBA/2 mice exhibit greater susceptibility to Mycoplasma pulmonis infection, showing increased bacterial growth and inflammation. This hyper-immune response in susceptible mice, like DBA/2, contrasts with resistant C57BL/6 mice.
Area of Science:
- Immunology
- Microbiology
- Infectious Diseases
Background:
- Mycoplasma infections cause significant respiratory issues globally in humans and animals.
- Murine respiratory mycoplasmosis is a common disease model, with varying susceptibility observed in different mouse strains.
- Understanding strain-specific immune responses is crucial for managing Mycoplasma pulmonis (M. pulmonis) infections.
Purpose of the Study:
- To compare cellular immune responses between resistant C57BL/6NCrSlc (B6) and susceptible DBA/2CrSlc (D2) mice following M. pulmonis infection.
- To elucidate the immunological basis for differential susceptibility to murine respiratory mycoplasmosis.
Main Methods:
- Infection of B6 and D2 mice with M. pulmonis.
- Quantification of bacterial load in lung tissue.
- Analysis of pulmonary immune cell infiltration (neutrophils, macrophages, lymphocytes).
- Measurement of pro-inflammatory cytokines (IL-1β, IL-6, IL-17A, TNF-α) in bronchoalveolar lavage fluid.
Main Results:
- DBA/2 mice displayed significantly higher bacterial proliferation in the lungs compared to B6 mice.
- Increased infiltration of neutrophils, macrophages, and lymphocytes was observed in the lungs of D2 mice.
- Elevated levels of IL-1β, IL-6, IL-17A, and TNF-α were detected in bronchoalveolar lavage fluid from D2 mice.
Conclusions:
- DBA/2 mice are more susceptible to M. pulmonis infection than B6 mice.
- A hyper-inflammatory immune response characterized by elevated cytokine production and immune cell infiltration contributes to the susceptibility of D2 mice.
- These findings highlight the role of host immune response in the pathogenesis of murine respiratory mycoplasmosis.
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