ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2026
Lipopolysaccharide promotes rheumatoid arthritis by enhancing Wnt7b mediated macrophage-FLS communication.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundOur previous research has shown that lipopolysaccharide (LPS) derived from Gram-negative bacteria in the intestine promoted rheumatoid arthritis (RA) after entering peripheral blood, but the specific molecular mechanism was unclear.
methodThis study used transcriptome and proteomic sequencing, western blotting, co-immunoprecipitation (Co-IP), cell co-culture, and other related methods to investigate whether LPS entering peripheral blood activated the Wnt7b secretion in macrophages, and used the Wnt7b as a messenger molecule to promote the communication between macrophage-fibroblast-like synoviocyte (FLSs), ultimately leading to the onset of RA.
resultThe results showed that LPS significantly promoted the pathology of collagen induced arthritis (CIA) mice. Transcriptome and proteomic sequencing, as well as experimental validation, confirmed that the target of LPS may be the Wnt7b. Knocking down the Wnt7b in CIA mice could effectively alleviate the LPS induced pathology. Furthermore, in the M
conclusionThis study suggested that circulating LPS stimulated macrophages to secrete Wnt7b, which acted as a messenger molecule and bound to the FZD8 receptor on the FLSs cell membrane in the synovial microenvironment, promoting the activation of the Wnt/β-catenin signaling pathway in FLSs and leading to RA.
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