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Tau deficiency inhibits classically activated macrophage polarization and protects against collagen-induced arthritis in mice

Authors :
Meng Chen
Wenyu Fu
Huiyun Xu
Chuan-ju Liu
Source :
Arthritis Research & Therapy, Vol 25, Iss 1, Pp 1-10 (2023)
Publication Year :
2023
Publisher :
BMC, 2023.

Abstract

Abstract Background Tau protein serves a pro-inflammatory function in neuroinflammation. However, the role of tau in other inflammatory disorders such as rheumatoid arthritis (RA) is less explored. This study is to investigate the role of endogenous tau and the potential mechanisms in the pathogenesis of inflammatory arthritis. Methods We established collagen-induced arthritis (CIA) model in wild-type and Tau-/- mice to compare the clinical score and arthritis incidence. Micro-CT analysis was used to evaluate bone erosion of ankle joints. Histological analysis was performed to assess inflammatory cell infiltration, cartilage damage, and osteoclast activity in the ankle joints. Serum levels of pro-inflammatory cytokines were measured by ELISA. The expression levels of macrophage markers were determined by immunohistochemistry staining and quantitative real-time PCR. Results Tau expression was upregulated in joints under inflammatory condition. Tau deletion in mice exhibited milder inflammation and protected against the progression of CIA, evidenced by reduced serum levels of pro-inflammatory cytokines and attenuated bone loss, inflammatory cell infiltration, cartilage damage, and osteoclast activity in the ankle joints. Furthermore, tau deficiency led to the inhibition of classically activated type 1 (M1) macrophage polarization in the synovium. Conclusion Tau is a previously unrecognized critical regulator in the pathogenesis of RA and may provide a potential therapeutic target for autoimmune and inflammatory joint diseases.

Details

Language :
English
ISSN :
14786362
Volume :
25
Issue :
1
Database :
Directory of Open Access Journals
Journal :
Arthritis Research & Therapy
Publication Type :
Academic Journal
Accession number :
edsdoj.8ff9095114df48bbb26a98735e1940e9
Document Type :
article
Full Text :
https://doi.org/10.1186/s13075-023-03133-4