Does lipopolysaccharide-mediated inflammation have a role in OA?

Journal Article (Journal Article;Review)

The nature of the gastrointestinal microbiome determines the reservoir of lipopolysaccharide, which can migrate from the gut into the circulation, where it contributes to low-grade inflammation. Osteoarthritis (OA) is a low-grade inflammatory condition, and the elevation of levels of lipopolysaccharide in association with obesity and metabolic syndrome could contribute to OA. A 'two- hit' model of OA susceptibility and potentiation suggests that lipopolysaccharide primes the proinflammatory innate immune response via Toll-like receptor 4 and that progression to a full-blown inflammatory response and structural damage of the joint results from coexisting complementary mechanisms, such as inflammasome activation or assembly by damage-associated molecular patterns in the form of fragmented cartilage-matrix molecules. Lipopolysaccharide could be considered a major hidden risk factor that provides a unifying mechanism to explain the association between obesity, metabolic syndrome and OA.

Full Text

Duke Authors

Cited Authors

  • Huang, Z; Kraus, VB

Published Date

  • February 2016

Published In

Volume / Issue

  • 12 / 2

Start / End Page

  • 123 - 129

PubMed ID

  • 26656661

Pubmed Central ID

  • PMC4930555

Electronic International Standard Serial Number (EISSN)

  • 1759-4804

Digital Object Identifier (DOI)

  • 10.1038/nrrheum.2015.158


  • eng

Conference Location

  • United States