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Pathogenetic mechanisms in the Mycoplasma arthritidis polyarthritis of rats
H Kirchhoff1, A Binder, M Runge
1Institut für Mikrobiologie und Tierseuchen, Tierärztliche Hochschule, Hannover, Federal Republic of Germany.
Abstract:
Mycoplasma arthritidis is the causative agent of severe polyarthritis in rats and mice, which resembles human rheumatoid arthritis (RA). Several mechanisms are involved in this disease. M. arthritidis releases substances acting on polymorphonuclear granulocytes (PMNs), i.e. oxygen radical formation stimulating substances (500-3,000 daltons), a chemotactic substance (400 daltons) and an aggregating substance (500 daltons). These products were separated from the cell-free culture supernatant by gel chromatography on Sephadex G-15 and G-10 columns. Isolated membranes of M. arthritidis possesses toxic properties for rats, mice, and chicken embryos. Hemolytic activities for sheep red blood cells and toxic effects on fetal rat skin fibroblasts were detected for this 170,000 dalton substance. Cross-reactivity between M. arthritidis and rat tissues was demonstrated in several investigations with polyclonal and monoclonal antibodies. Polyclonal antibodies against M. arthritidis showed a strong reaction in immunofluorescence tests with rat chondrocytes. In Western blot analysis six corresponding protein bands were observed in M. arthritidis membranes and rat chondrocytes, favoring the idea of several shared epitopes. Monoclonal antibodies were established reacting with M. arthritidis as well as with rat and human chondrocytes in the immunofluorescence test and in the enzyme immunoassay. Cross-reactivity could be observed also on the cellular level. T-cell lines of the OX 19 and W 3/25 type were established that could be stimulated by M. arthritidis antigens and by syngeneic chondrocytes. In the initial stage of the arthritis, toxic processes seem to be predominant that are continued by autoimmune reactions in the progressing disease.
Insights
Mycoplasma arthritidis infection causes severe arthritis in rodents, mimicking human rheumatoid arthritis. The study reveals toxic effects and molecular mimicry, suggesting autoimmune triggers in disease progression.
Area of Science:
- Immunology
- Microbiology
- Rheumatology
Background:
- Mycoplasma arthritidis causes severe polyarthritis in rodents, a model for human rheumatoid arthritis.
- The disease involves complex mechanisms including microbial products affecting immune cells.
Purpose of the Study:
- To investigate the mechanisms by which Mycoplasma arthritidis induces arthritis.
- To explore the role of molecular mimicry in the pathogenesis of M. arthritidis-induced arthritis.
Main Methods:
- Gel chromatography was used to isolate M. arthritidis-derived substances.
- Isolated membranes and antibodies were used to assess toxicity and cross-reactivity.
- Immunofluorescence, Western blot, and enzyme immunoassays were employed to study cellular interactions.
Main Results:
- M. arthritidis releases substances that stimulate polymorphonuclear granulocytes and exhibit chemotactic and aggregating properties.
- Isolated M. arthritidis membranes showed toxicity to various cells and tissues.
- Significant cross-reactivity was observed between M. arthritidis antigens and rat/human chondrocytes, indicating shared epitopes.
- T-cell lines were stimulated by both M. arthritidis antigens and syngeneic chondrocytes.
Conclusions:
- Mycoplasma arthritidis employs toxic mechanisms and molecular mimicry to induce arthritis.
- Autoimmune reactions, potentially triggered by shared epitopes, contribute to the progression of the disease.