Abstract
Rheumatoid arthritis is an autoimmune disease that affects human beings worldwide. Infections have been associated to autoimmune diseases because their ability to induce a dominant cytokine response. Joint inflammation has been related to Th1 response because they induce high expression of proinflammatory cytokines TNF-α, IL-1, IFN-γ. MRL/lpr mice spontaneously develop an autoimmune disease affecting joints, kidneys, etc. We compared incidence and severity of arthritis, antibody response, cytokine production, in mice infected with bacteria or helminthes in the Murphy Roths Large (MRL)lpr mice. Infections with helminthes Heligmosomoides polygyrus, Nippostrongylus brasiliensis or bacteria Nocardia brasiliensis and Staphylococcus aureus were studied. IL-4, IFN-γ and IgG1, IgG2a antibody productions were determined. IFN-γ was increased in all groups, the highest production was observed after bacterial infection; IL-4 production was higher after helminthes infection. IgG1 sera levels were increased in the helminthes infected group. IgG2a sera concentration was stimulated by bacterial infection. The histopathology showed that 100% of bacterial infected mice developed arthritis and severe tissue damage such as cartilage erosion and bone destruction. Animals infected with parasites showed a decreased incidence and severity of arthritis. Severity of tissue damage in joints is correlated with increased numbers of lymphocytes and macrophages immunoreactive to proinflammatory cytokines.
Acknowledgements
This work was supported by Grant # 47542 from CONACYT Mexico and PAICYT, UANL, Monterrey, México. This work fulfills part of the requirements for a PhD degree by Guadalupe de la Cruz-Galicia. Our thanks to Mr Reynaldo Rodriguez for technical assistance with animals care. We are grateful to Dr Joseph F. Urban, Jr. for kindly donating the parasites. Our thanks go to José Angel Garza for English corrections.
Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.