Published online Apr 6, 2021. doi: 10.12998/wjcc.v9.i10.2181
Peer-review started: December 11, 2020
First decision: December 30, 2020
Revised: January 13, 2021
Accepted: February 11, 2021
Article in press: February 11, 2021
Published online: April 6, 2021
Processing time: 108 Days and 23 Hours
The role of macrophages in rheumatoid arthritis (RA) and its mechanism have attracted much attention in RA pathogenesis.
To investigate the effects of Iguratimod on the polarity of mononuclear macrophages in elderly patients with RA.
Macrophages accumulate in the synoviums of RA, and the proportion of M1 type pro-inflammatory macrophages is higher than that of M2 type anti-inflammatory macrophages, leading to the secretion of inflammatory molecules and the aggravation of inflammatory reaction, which makes macrophages potential targets of RA drugs.
Elderly patients with RA and joint effusion were selected. Patients were treated with oral administration of 25 mg Iguratimod (Iremod, Iremod, State Food and Drug Administration Approval No. H20110084). Venous blood and joint effusion fluid were collected, mononuclear macrophages were extracted, and expression of cell surface markers CD86, CD64, CD163, and CD206 was analyzed by flow cytometry. The concentration of inflammatory factors interleukin (IL)-6, IL-1β, transforming growth factor-β, and IL-4 in the joint effusion fluid was analyzed by enzyme-linked immunosorbent assay. Expression of mononuclear cells inhibitor of nuclear factor-κB (IκB) and phosphorylated IκB in peripheral blood was analyzed by western blotting.
Western blot analysis showed that mononuclear cell IκB in peripheral blood was significantly increased after treatment, and its phosphorylation level was significantly decreased (P < 0.05).
Iguratimod can promote the transformation of mononuclear macrophages from M1 to M2 in elderly patients with RA by inhibiting the nuclear factor-κB (NF-κB) pathway, thus improving symptoms of RA. Iguratimod can promote the transformation of mononuclear macrophages from M1 to M2 in elderly patients with RA. Iguratimod promotes the transformation of mononuclear macrophages from M1 to M2 by decreasing phosphorylation level of IκB
First, because of the small number of joint effusion fluid samples, only the activation of the NF-κB pathway in peripheral blood mononuclear cells was detected, and activation of the NF-κB pathway in joint effusion fluid macrophages needs further research. Second, the specific mechanism of Iguratimod regulation of the NF-κB pathway has not yet been elucidated.