In a study on the causes of some forms of arthritis in animals, researchers now have shown that both a bacterial trigger and genetic susceptibility are necessary for the disease to occur. This discovery results from a study to determine if a human gene, HLA-B27, was the major cause of a group of rheumatic disorders called spondyloarthropathies.
Earlier studies showed that rats carrying the human HLA-B27 gene developed joint inflammation (arthritis) and other symptoms characteristic of human spondyloarthropathies. In an article in the December issue of Journal of Experimental Medicine, researchers report that when these B27 transgenic rats are raised in a germ-free environment, they no longer develop arthritis. People who inherit the HLAB27 gene have a markedly increased risk of developing one of the spondyloarthropathic disorders.
Arthritis researchers believe that many rheumatic diseases result from a combination of genetic factors that determine susceptibility and bacterial or other environmental triggers. Researchers already know that some forms of spondyloarthropathies, termed reactive arthritis, are triggered by certain types of inflections, particularly in individuals with HLA-B27. Once researchers find the specific types of bacteria that trigger arthritis, the researchers plan to study the immune response to these bacteria in HLA-B27 rats and normal rats.