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Strain-Specific Variation of the Decorin-Binding Adhesin DbpA Influences the Tissue Tropism of the Lyme Disease Spirochete
Lyme disease, the most common vector-borne disease in the United States, is caused by a bacterium, Borrelia burgdorferi. This bacterium infects the skin at the site of the tick bite and then can spread to other tissues, such as the heart, joints or nervous system, causing carditis, arthritis or neurologic disease. To colonize human tissues, the pathogen produces surface proteins that promote bacterial attachment to these sites. For example, DbpA binds to decorin, a component of human tissue. Different Lyme disease strains differ in the particular tissues they colonize and the disease they cause, but we do not understand why. Different strains also make distinct versions of DbpA that bind decorin differently, so variation of DbpA might contribute to strain-to-strain variation in clinical manifestations. To test this, we infected mice with Lyme disease strains that were identical except for the particular DbpA variant they produced. We found that the strains colonized different tissues and caused different diseases, such as arthritis or carditis. These results provide the first solid evidence that variation of an outer surface protein, in this case DbpA, influences what tissues are most affected during Lyme disease.
Vyšlo v časopise: Strain-Specific Variation of the Decorin-Binding Adhesin DbpA Influences the Tissue Tropism of the Lyme Disease Spirochete. PLoS Pathog 10(7): e32767. doi:10.1371/journal.ppat.1004238
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1004238Souhrn
Lyme disease, the most common vector-borne disease in the United States, is caused by a bacterium, Borrelia burgdorferi. This bacterium infects the skin at the site of the tick bite and then can spread to other tissues, such as the heart, joints or nervous system, causing carditis, arthritis or neurologic disease. To colonize human tissues, the pathogen produces surface proteins that promote bacterial attachment to these sites. For example, DbpA binds to decorin, a component of human tissue. Different Lyme disease strains differ in the particular tissues they colonize and the disease they cause, but we do not understand why. Different strains also make distinct versions of DbpA that bind decorin differently, so variation of DbpA might contribute to strain-to-strain variation in clinical manifestations. To test this, we infected mice with Lyme disease strains that were identical except for the particular DbpA variant they produced. We found that the strains colonized different tissues and caused different diseases, such as arthritis or carditis. These results provide the first solid evidence that variation of an outer surface protein, in this case DbpA, influences what tissues are most affected during Lyme disease.
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