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Do infectious agents cause rheumatoid arthritis?
1Arthritis and Rheumatism Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892.
Abstract:
Although rheumatoid arthritis (RA) has been widely suspected to have an infectious etiology, this hypothesis has remained difficult to prove. Epstein-Barr virus, parvoviruses, and retroviruses are considered by some investigators to be the primary candidates. An increasing body of data, on the other hand, appears to implicate bacteria or their products in the syndrome. Important evidence has surfaced in support of this view. Lyme arthritis, a disease caused by a bacterium, can mimic RA. Bacteria and their products have been conclusively linked to many forms of inflammatory "reactive" arthropathies. RA-like diseases can be induced in certain inbred strains of rats with bacterial cell-wall fragments, e.g., streptococcal and other bacterial peptidoglycans. Immunologic relationships between host and bacterial peptidoglycans, relevant to RA, have been well documented, e.g., heat shock proteins, bacterial IgG Fc binding proteins, and rheumatoid factors. These data not only support the hypothesis that bacteria may play an important role in RA but also indicate that current concepts of infection and autoimmune disease are broadening and overlapping.
Insights
Evidence suggests bacteria, not just viruses, may cause rheumatoid arthritis (RA). Bacterial products and immune responses mimic RA, indicating a potential infectious link to this autoimmune disease.
Area of Science:
- Immunology
- Microbiology
- Rheumatology
Background:
- Rheumatoid arthritis (RA) has long been suspected to have an infectious origin, but definitive proof remains elusive.
- Viruses like Epstein-Barr virus and parvoviruses have been considered potential culprits.
- Emerging data increasingly points towards a bacterial etiology for RA.
Purpose of the Study:
- To explore the evidence implicating bacteria in the pathogenesis of rheumatoid arthritis.
- To investigate the immunological links between bacterial components and RA-like conditions.
Main Methods:
- Review of existing literature on infectious agents and arthritis.
- Examination of animal models of RA induced by bacterial products.
- Analysis of immunological cross-reactivity between bacterial antigens and host components relevant to RA.
Main Results:
- Lyme arthritis, caused by bacteria, can clinically resemble RA.
- Bacterial products are definitively linked to various inflammatory reactive arthropathies.
- Bacterial cell-wall fragments (peptidoglycans) can induce RA-like diseases in rats.
- Immunological connections, including heat shock proteins and rheumatoid factors, exist between bacterial peptidoglycans and RA.
Conclusions:
- The hypothesis that bacteria play a significant role in RA is supported by substantial evidence.
- These findings suggest a broadening understanding of autoimmune diseases, with increasing overlap with infectious processes.
- Current concepts of infection and autoimmunity are evolving to encompass shared mechanisms.