Decorin as a conduit for Lyme disease bacteria

As Lyme disease progresses past the early stage of a rash in the region of the initial infection, spirochetes circulate throughout the body and infect various organs. Lyme arthritis occurs when the pathogens colonize the joints, and Brown and colleagues have now identified a molecular interaction between host and pathogen that seems to be particularly important for this aspect of the disease. Borrelia burgdorferi spirochetes interact with host ECM components through multiple adhesive receptors, including two surface proteins that bind specifically to decorin, a proteoglycan associated with interstitial collagen in the skin and cartilage. Decorin-deficient mice show only relatively subtle phenotypes in most respects, and when they are infected with Borrelia, either by direct injection or by being bitten by infected ticks, the spirochetes become disseminated to most tissues at nearly normal levels. Nevertheless, the absence of decorin confers on these animals a significant protection from Lyme arthritis, especially at low doses of bacteria. These mutant mice are similar to wild-type animals in their immune responses to Borrelia and in their sensitivity to other forms of pathogen-induced arthritis, suggesting that adhesion to decorin is specifically involved in disseminating the spirochete to the joints of infected animals.