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.

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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