Published online Sep 28, 2023. doi: 10.3748/wjg.v29.i36.5226
Peer-review started: August 16, 2023
First decision: August 25, 2023
Revised: August 26, 2023
Accepted: September 7, 2023
Article in press: September 7, 2023
Published online: September 28, 2023
Processing time: 35 Days and 5.5 Hours
Restoration of immune homeostasis by targeting the balance between memory T helper (mTh) cells and memory follicular T helper (mTfh) cells is a potential therapeutic strategy against ulcerative colitis (UC). Because of its anti-inflammatory and immunomodulatory properties, curcumin (Cur) is a promising drug for UC treatment. However, fewer studies have demonstrated whether Cur can modulate the mTh/mTfh subset balance in mice with colitis.
To explore the potential mechanism underlying Cur-mediated alleviation of colitis induced by dextran sulfate sodium (DSS) in mice by regulating the mTh and mTfh immune homeostasis.
Balb/c mice were administered 3% and 2% DSS to establish the UC model and treated with Cur (200 mg/kg/d) by gavage on days 11-17. On the 18th d, all mice were anesthetized and euthanized, and the colonic length, colonic weight, and colonic weight index were evaluated. Histomorphological changes in the mouse colon were observed through hematoxylin-eosin staining. Levels of Th/mTh and Tfh/mTfh cell subsets in the spleen were detected through flow cytometry. Western blotting was performed to detect SOCS-1, SOCS-3, STAT3, p-STAT3, JAK1, p-JAK1, and NF-κB p65 protein expression levels in colon tissues.
Cur effectively mitigates DSS-induced colitis, facilitates the restoration of mouse weight and colonic length, and diminishes the colonic weight and colonic weight index. Simultaneously, it hinders ulcer development and inflammatory cell infiltration in the colonic mucous membrane. While the percentage of Th1, mTh1, Th7, mTh7, Th17, mTh17, Tfh1, mTfh1, Tfh7, mTfh7, Tfh17, and mTfh17 cells decreased after Cur treatment of the mice for 7 d, and the frequency of mTh10, Th10, mTfh10, and Tfh10 cells in the mouse spleen increased. Further studies revealed that Cur administration prominently decreased the SOCS-1, SOCS-3, STAT3, p-STAT3, JAK1, p-JAK1, and NF-κB p65 protein expression levels in the colon tissue.
Cur regulated the mTh/mTfh cell homeostasis to reduce DSS-induced colonic pathological damage, potentially by suppressing the JAK1/STAT3/SOCS signaling pathway.
Core Tip: Memory T cells (mTh) are formed by the differentiation of initial T cells following antigenic stimulation and have a long lifespan. The dysfunction and out-of-balance of mTh and their subsets destroy immune homeostasis to induce autoimmune diseases including inflammatory bowel disease. Finding new drugs for inflammatory bowel disease (IBD) treatment from natural plant medicine and traditional Chinese medicine is a research hotspot. Cur can regulate memory B cells and other immune cells to effectively treat experimental colitis. However, whether Cur can regulate mTh cell- and mfTh cell-mediated homeostasis to treat IBD remains unclear. We here indicated that Cur regulates the mTh/memory follicular T helper cell homeostasis to reduce dextran sulfate sodium-induced colonic pathological injury, which may be achieved by inhibiting the JAK1/STAT3/SOCS signaling pathway.