Psychological Stress Triggers Arthritis Flares in Mice via IL-6-Dependent Pathway
A study in mice offers up a biological explanation for how psychological stress can contribute to arthritis flares, and identifies a stress-responsive pathway that could be explored as a potential therapeutic target. The post Psychological Stress Triggers Arthritis Flares in Mice via IL-6-Dependent Pathway appeared first on GEN - Genetic Engineering and Biotechnology News .
Rheumatoid arthritis (RA) symptoms can worsen due to psychological stress, but the specific mechanism has been unclear. A study from Chiba University in mice suggests that psychological stress can reactivate arthritis by activating a stress-responsive pathway. This pathway involves the sympathetic nervous system, brown adipose tissue (BAT), and an inflammatory signaling protein called interleukin-6 (IL-6).
When exposed to restraint stress, mice with antigen-induced arthritis experienced a flare-up of joint inflammation. The stress activated BAT to release IL-6, which then stimulated fibroblast-like synoviocytes (FLS) in the joints. IL-6 triggered the production of CXCL1, a chemokine that attracted neutrophils, further contributing to the reactivation of joint inflammation.
Blocking the CXCR2 receptor, which responds to CXCL1, significantly reduced stress-induced arthritis in the mouse model. These findings suggest that targeting the stress-responsive pathways could be a potential therapeutic strategy for managing RA without broadly suppressing the immune system.
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