Does lipopolysaccharide-mediated inflammation have a role in OA?
Does lipopolysaccharide-mediated inflammation have a role in OA?
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DOI：
10.1038/nrrheum.2015.158
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发表时间：
2016-02
期刊：
影响因子：
--
通讯作者：
Kraus VB
中科院分区：
文献类型：
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作者：
Huang Z;Kraus VB
胃肠道微生物组的性质决定了脂多糖（LPS）的储存库，脂多糖可以从肠道迁移到循环中，在那里它有助于低度炎症。骨关节炎（OA）是一种低度炎症性疾病，与肥胖和代谢综合征相关的LPS水平升高可能导致OA。OA易感性和增强作用的双因子模型表明，LPS通过Toll样受体4引发促炎性先天免疫应答，并且进展为全面的炎症反应和关节结构损伤是由共存的互补机制引起的，例如炎性小体激活或以片段化软骨基质分子形式的损伤相关分子模式组装。LPS可以被认为是一个主要的隐藏的危险因素，提供了一个统一的机制来解释肥胖，代谢综合征和OA之间的关联。
The nature of the gastrointestinal microbiome determines the reservoir of lipopolysaccharide (LPS), 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 LPS in association with obesity and metabolic syndrome could contribute to OA. A bifactorial model of OA susceptibility and potentiation suggests that LPS 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. LPS could be considered a major hidden risk factor that provides a unifying mechanism to explain the association between obesity, metabolic syndrome and OA.