Hydroquinone Exposure Worsens Rheumatoid Arthritis through the Activation of the Aryl Hydrocarbon Receptor and Interleukin-17 Pathways
نویسندگان
چکیده
Rheumatoid arthritis (RA) development is strongly associated with cigarette smoke exposure, which activates the aryl hydrocarbon receptor (AhR) as a trigger for Th17 inflammatory pathways. We previously demonstrated that exposure to hydroquinone (HQ), one of major compounds tar, aggravates symptomatology in rats. However, mechanisms related HQ-related RA still remain elusive. Cell viability, cytokine secretion, and gene expression were measured human fibroblast-like synoviocytes (RAHFLS) treated HQ stimulated or not TNF-α. Antigen-induced (AIA) was also elicited wild type (WT), AhR −/− IL-17R C57BL/6 mice upon daily nebulized (25ppm) between days 15 21. At day 21, challenged mBSA parameters assessed. The vitro treatment up-regulated TNFR1, TNFR2 expression, increased ROS production. co-treatment TNF-α enhanced IL-6 IL-8 secretion. pre-incubation RAHFLS an antagonist inhibited HQ-mediated cell proliferation profile. About vivo approach, worsened AIA symptoms (edema, pain, cytokines secretion NETs formation) WT mice. These effects abolished HQ-exposed animals though. Our data harmful influence over onset through activation synoviocytes. severity IL-17 pathways, highlighting how can contribute progression.
منابع مشابه
Aryl hydrocarbon receptor antagonism and its role in rheumatoid arthritis.
Although rheumatoid arthritis (RA) is the most common autoimmune disease, affecting approximately 1% of the population worldwide, its pathogenic mechanisms are poorly understood. Tobacco smoke, an environmental risk factor for RA, contains several ligands of aryl hydrocarbon receptor (Ahr), also known as dioxin receptor. Ahr plays critical roles in the immune system. We previously demonstrated ...
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ژورنال
عنوان ژورنال: Antioxidants
سال: 2021
ISSN: ['2076-3921']
DOI: https://doi.org/10.3390/antiox10060929