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Borrelia burgdorferi?BbHtrA degrades host ECM proteins and stimulates release of inflammatory cytokines in vitro.

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Abstract

The
Lyme disease spirochaete, Borrelia burgdorferi, causes damage to diverse host tissues and induces inflammation but the mechanisms of injury are poorly understood. We recently reported that a surface-exposed B.?burgdorferi protease, which is expressed during human
disease and is conserved within the major
Lyme disease spirochaete species, degrades the extracellular matrix proteoglycan, aggrecan. Here we demonstrate that BbHtrA also degrades fibronectin and numerous proteoglycans found in skin, joints and neural tissues. BbHtrA degradation of fibronectin released known pro-inflammatory fibronectin fragments FnIII(13-14) and Fnf-29, which may amplify the inflammatory processes triggered by the presence of the bacteria. When this hypothesis was tested directly by exposing chondrocytes to BbHtrA?in vitro, inflammatory cytokines (sICAM-1 and IL-6) and chemokines (CXCL1, CCL1, CCL2 and CCL5) that are hallmarks of
Lyme disease were induced. These results provide the first evidence that, by utilizing BbHtrA, B.?burgdorferi may actively participate in its dissemination and in the tissue damage and inflammation observed in
Lyme disease.

Published 2013. This article is a U.S. Government work and is in the public domain in the USA.

Mol Microbiol. 2013 Oct;90(2):241-51. doi: 10.1111/mmi.12377. Epub 2013 Sep 16. Research Support, Non-U.S. Gov’t

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