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Updated: Jul 1, 2026

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Published on: June 6, 2025
Association of Mycoplasma arthritidis mitogen with lethal toxicity but not with arthritis in mice
Wenyi Luo1, Huilan Yu, Zuhua Cao
1Department of Genetics, University of Alabama at Birmingham, Birmingham, AL 35294-0024, USA.
Abstract:
Mycoplasma arthritidis induces an acute to chronic arthritis in rodents. Arthritis induced in mice histologically resembles human rheumatoid arthritis and can be associated with lethal toxicity following systemic injection. The M. arthritidis mitogen (MAM) superantigen has long been implicated as having a role in pathogenesis, but its significance with respect to toxicity and arthritogenicity in mycoplasma-induced disease is unclear. To study the pathogenic significance of MAM, M. arthritidis mutants that overproduced or failed to produce MAM were developed. MAM overproduction and knockout mutants were more and less mitogenic, respectively, than the wild-type strain. The degree of mitogenic activity correlated with lethal toxicity in DBA/2J mice. In contrast, histopathological studies detected no correlation between MAM production and the severity of arthritis induced in DBA/2J and CBA/J mice.
Insights
Mycoplasma arthritidis superantigen (MAM) influences lethal toxicity in mice, but does not correlate with arthritis severity. This study clarifies MAM
Area of Science:
- Immunology
- Microbiology
- Rheumatology
Background:
- Mycoplasma arthritidis causes arthritis in rodents, mimicking human rheumatoid arthritis.
- The role of Mycoplasma arthritidis mitogen (MAM) in disease pathogenesis, toxicity, and arthritogenicity remains unclear.
Purpose of the Study:
- To investigate the pathogenic significance of MAM in M. arthritidis-induced disease.
- To determine the correlation between MAM production, lethal toxicity, and arthritis severity.
Main Methods:
- Development of M. arthritidis mutants with altered MAM production (overproduction and knockout).
- Assessment of mitogenic activity, lethal toxicity in DBA/2J mice, and arthritis severity in DBA/2J and CBA/J mice via histopathology.
Main Results:
- MAM overproduction and knockout mutants exhibited higher and lower mitogenic activity, respectively, compared to the wild-type strain.
- A direct correlation was observed between the degree of mitogenic activity and lethal toxicity in DBA/2J mice.
- No correlation was found between MAM production levels and the severity of induced arthritis in either mouse strain.
Conclusions:
- MAM plays a significant role in the lethal toxicity of M. arthritidis infections.
- MAM production is not a determining factor in the arthritogenicity of M. arthritidis.
