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Expression of metabolism-inhibition antibodies against Mycoplasma arthritidis in rats
L R Washburn1, B C Cole, J R Ward
1Department of Medicine, School of Medicine, Salt Lake City 84132.
Abstract:
Shared antigens between Mycoplasma arthritidis and rat tissues may be responsible for the lack of metabolism-inhibition (MI) and other neutralizing antibodies in rats with M arthritidis-induced arthritis. We were not able to confirm such antigens or to detect cross-reacting antigens between M arthritidis and rat lymphocytes, thymocytes, and muscle tissue. Antisera of rabbit origin to rat lymphocytes, thymocytes, and skeletal muscle reacted by ELISA with M arthritidis only when the mycoplasmal antigens were prepared from organisms grown in medium containing horse serum. Such activity could be completely absorbed by horse serum. These antisera to rat tissues also failed to react by radioimmunoprecipitation with M arthritidis surface antigens. In addition, antibody activity against homologous antigens could not be absorbed by M arthritidis. Similarly, antisera of rabbit origin against M arthritidis failed to react by ELISA specifically with rat lymphocytes, thymocytes, and skeletal muscle or to react by radioimmunoprecipitation with 125I-labeled rat lymphocyte antigens. These rat tissues could not specifically absorb antibodies against M arthritidis from antisera of rabbit origin. These findings suggest that the lack of MI antibodies in rats probably can not be explained by rat tissue antigens that cross-react with M arthritidis MI antigens. Finally, antisera of rat origin against M arthritidis and other rat tissue components failed to block rabbit MI activity against M arthritidis, thus arguing against steric hindrance as a means of preventing recognition of MI antigens.
Insights
Shared antigens were investigated as a cause for the lack of metabolism-inhibition (MI) antibodies in rats with Mycoplasma arthritidis arthritis. Studies found no evidence of cross-reacting antigens between the bacteria and rat tissues, refuting this hypothesis.
Area of Science:
- Immunology
- Microbiology
- Rheumatology
Background:
- Mycoplasma arthritidis-induced arthritis in rats is often associated with a lack of metabolism-inhibition (MI) and other neutralizing antibodies.
- A potential explanation involves shared antigens between Mycoplasma arthritidis and rat tissues, leading to immune tolerance or non-responsiveness.
Purpose of the Study:
- To investigate the hypothesis that shared antigens between Mycoplasma arthritidis and rat tissues are responsible for the absence of neutralizing antibodies in rats.
- To determine if cross-reactivity exists between Mycoplasma arthritidis and rat lymphocytes, thymocytes, and muscle tissue.
Main Methods:
- Enzyme-linked immunosorbent assay (ELISA) was used to detect antibody binding between antisera and antigens.
- Radioimmunoprecipitation was employed to assess surface antigen interactions.
- Absorption assays were performed to confirm antigen specificity and rule out cross-reactivity.
Main Results:
- No cross-reacting antigens were detected between Mycoplasma arthritidis and rat lymphocytes, thymocytes, or muscle tissue.
- Antibody reactivity observed with Mycoplasma arthritidis using antisera to rat tissues was attributed to horse serum contamination and was fully absorbed by horse serum.
- Antisera against Mycoplasma arthritidis did not react with rat tissues, and rat tissues did not absorb antibodies against Mycoplasma arthritidis.
Conclusions:
- The lack of metabolism-inhibition (MI) antibodies in rats with Mycoplasma arthritidis-induced arthritis cannot be explained by shared antigens between the bacterium and rat tissues.
- Immune responses in this model are not hindered by steric hindrance or cross-reactivity with host tissue antigens.