Related Experiment Videos
Chronic respiratory mycoplasmosis in C3H/HeN and C57BL/6N mice: lesion severity and antibody response
S C Cartner1, J W Simecka, J R Lindsey
1Department of Comparative Medicine, University of Alabama at Birmingham 35294-0019, USA.
Abstract:
Mycoplasma pneumoniae is a leading, worldwide cause of death and disability due to pneumonia. Mycoplasma pulmonis infection in mice is an invaluable model for the study of host defenses against respiratory mycoplasmas in vivo. C3H/HeN mice are much more susceptible to acute inflammatory lung disease due to M. pulmonis than C57BL/6N mice, but little is known about the chronic disease in these mouse strains. We infected C3H/HeN and C57BL/6N mice with 10(4) CFU of M. pulmonis UAB CT and evaluated them at weekly intervals by quantitative mycoplasma culture of nasal passages, trachea, and lungs, assessment of lesion severity in nasal passages, trachea, and lungs, and determination of serum immunoglobulin classes and subclasses by enzyme-linked immunosorbent assay. We found that C3H/HeN mice had 2 to 5 logs more organisms in their lungs and far more severe lung disease than C57BL/6N mice through 63 days postinfection. Although both strains of mice developed the same classes of antibody, C3H/HeN mice had much greater anti-M. pulmonis immunoglobulin G (IgG) responses in the IgG1 and IgG2a subclasses than C57BL/6N mice. These results suggest that adaptive immunity does not effect resolution of chronic mycoplasma infection and disease in the lungs.
Insights
Susceptible C3H/HeN mice develop severe chronic lung disease and higher immunoglobulin G responses to Mycoplasma pulmonis compared to resistant C57BL/6N mice, indicating adaptive immunity may not resolve this infection.
Area of Science:
- Immunology
- Microbiology
- Pulmonology
Background:
- Mycoplasma pneumoniae causes significant pneumonia globally.
- Mycoplasma pulmonis infection in mice serves as a key model for studying respiratory mycoplasma host defenses.
- C3H/HeN mice exhibit greater susceptibility to acute Mycoplasma pulmonis-induced lung inflammation than C57BL/6N mice, with limited data on chronic disease.
Purpose of the Study:
- To investigate the chronic Mycoplasma pulmonis disease progression and host immune responses in susceptible C3H/HeN and resistant C57BL/6N mice.
- To compare the severity of lung lesions and mycoplasma burden between the two mouse strains.
- To analyze the differences in immunoglobulin G subclass responses in relation to disease outcome.
Main Methods:
- Infection of C3H/HeN and C57BL/6N mice with Mycoplasma pulmonis UAB CT.
- Weekly quantitative cultures of nasal passages, trachea, and lungs.
- Assessment of lesion severity in respiratory tissues.
- Enzyme-linked immunosorbent assay to determine serum immunoglobulin classes and subclasses.
Main Results:
- C3H/HeN mice demonstrated significantly higher mycoplasma loads (2-5 logs) and more severe lung disease up to 63 days post-infection compared to C57BL/6N mice.
- Both mouse strains produced similar classes of antibodies.
- C3H/HeN mice exhibited markedly elevated anti-Mycoplasma pulmonis immunoglobulin G1 and IgG2a subclass responses.
Conclusions:
- Adaptive immunity does not appear to resolve chronic Mycoplasma pulmonis infection and associated lung disease.
- Differences in susceptibility between mouse strains correlate with distinct immunoglobulin G subclass responses.
- Further research is needed to understand mechanisms of chronic respiratory mycoplasma pathogenesis and resolution.