Does lipopolysaccharide-mediated inflammation have a role in OA?

Published

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

  • 26656661

Electronic International Standard Serial Number (EISSN)

  • 1759-4804

Digital Object Identifier (DOI)

  • 10.1038/nrrheum.2015.158

Language

  • eng

Conference Location

  • United States