Protective Role of Helminthiasis in the Development of Autoimmune Diseases

A role for microorganisms in the development of inflammatory arthropathies has long been recognized. Since the description of reactive arthritis, bacteria have been linked to bouts of arthritis that are thought to occur in a genetically susceptible host, after triggering by an infectious organism. In a recent article, Toivanen (2003) has proposed that arthritis results from bacteria encountered in the intestinal microbiota. Apparently, processed products of these bacteria gain access to the circulation and are entrapped in the joints, where immunocompetent cells, after being primed by these bacterial products, initiate and may then perpetuate an inflammatory response. Data to support this hypothesis are explored in that paper, as follows: arthritogenic bacteria usually are encountered in the gut. In addition, bacterial products were shown to promote synovitis experimentally and eradication of some infections may ameliorate or even abrogate the development of chronic synovitis. This microbiota hypothesis may also apply to certain viruses. The genetic component that is believed to be relevant in the pathogenesis of chronic arthritis is also contemplated in that “microbiota theory”. Indeed, differences in the intestinal flora were reported in patients with rheumatoid arthritis, as compared to healthy individuals. Also, genetic variations may account for differences in the intestinal microbiota. Other examples trying to substantiate this hypothesis are appearing in the literature. In a very recent paper, antibacterial peptide antibodies were proposed to be used as indices to support the diagnosis of rheumatoid arthritis and ankylosing spondylitis (Rashid et al. 2006). Though we consider this hypothesis very exciting, we will try to explore a somewhat opposite view. The contribution of genetics to the pathogenesis of inflammatory arthropathies cannot be overemphasized. However, to date, despite all the efforts made, the closer and most relevant association of a genetic component for arthritis refers to the human histocompatibility antigen HLA-B27 and the inflammatory spondyloarthropathies (Khan and Ball 2002). However, that association does not apply worldwide, as it is in white Caucasians. Actually, there are reports that some HLA-B27 variants, defined by the most recent molecular biology techniques, may even confer protection for the development of spondylitis (Khan and Ball 2002). The reduced coincidental prevalence of autoimmune disease among identical twins does also argue against a prominent genetic component in the pathogenesis of these entities. In rheumatoid arthritis, the concordance rate for twins varies from 15 to 30% (MacGregor et al. 2000). This does also apply for other autoimmune disorders such as insulin-dependent diabetes mellitus, where the concordance rate is around 40% (Hyttinen et al. 2003). The prevalence of rheumatoid arthritis is very similar worldwide. However, numbers appear to be a bit higher in developed countries, with a prevalence of 0.5–1.0%, whereas in underdeveloped countries this prevalence ranges from 0.1 to 0.5% (Alamanos and