Abstract
Immune memory is protective against reinvasion by pathogens in the homeostatic state, while immune memory disorders can cause autoimmune disease, including inflammatory bowel disease. Curcumin is a natural compound shown to be effective against human inflammatory bowel disease and experimental colitis, but the underlying mechanism is unclear. Here, experimental colitis was induced by dextran sulfate sodium (DSS) in this study. Significant changes in the percentages of naïve, central memory T (TCM), and effector memory (TEM) cells and their CD4+ and CD8+ subsets were found in the peripheral blood of mice with colitis using flow cytometry. After 7 days of continuous curcumin (100 mg/kg/day) administration, the DSS-induced experimental colitis was effectively relieved, with significant decreases in the ratio of day weight to initial body weight, colonic weight, pathological injury score, levels of proinflammatory cytokines IL-7, IL-15, and IL-21, colonic mucosal ulceration, and amount of inflammatory infiltrate. Importantly, curcumin significantly restored the percentages of naïve, TCM, and TEM cells and their CD4+ and CD8+ subpopulations. In addition, curcumin significantly inhibited the activation of the JAK1/STAT5 signaling pathway, downregulation of JAK1, STAT5, and p-STAT5 proteins in colon tissue, and upregulation of PIAS1 proteins. These results suggested that curcumin effectively regulated the differentiation of naïve, TCM, and TEM cells in the peripheral blood to alleviate DSS-induced experimental colitis, which might be related to the inhibition of JAK1/STAT5 signaling activity.
Highlights
Inflammatory bowel disease (IBD) refers to chronic autoimmune diseases of the gastrointestinal tract, including Crohn’s disease (CD) and ulcerative colitis (UC) (Hodson, 2016)
After dextran sulfate sodium (DSS) induction, the mice with colitis showed significant weight loss, hematochezia, and an increase in disease activity index score; colonic shortening, epithelial erosion of the colonic mucosa on microscopic examination, formation of ulcers and granulation tissue, disorganized crypt structure, and inflammatory cell infiltration; and a significant increase in the levels of proinflammatory cytokines IL-7, IL-15, and IL-21 in colonic tissues. These results suggested that DSS successfully recapitulated colitis
CD8+ TCM cells increased significantly; and the number of TEM and CD4+ TEM increased significantly, while CD8+ TEM cells decreased significantly. These results indicated that the numbers of memory T cells and their subsets significantly changed in DSSinduced colitis, suggesting that immune memory cell differentiation disorders might be closely related to the onset and development of IBD
Summary
Inflammatory bowel disease (IBD) refers to chronic autoimmune diseases of the gastrointestinal tract, including Crohn’s disease (CD) and ulcerative colitis (UC) (Hodson, 2016). IBD is a global disease with a high prevalence in developed countries (prevalence >0.3%) (Ungaro et al, 2017) and an accelerating prevalence in newly industrialized countries, especially in Asia (Ng et al, 2018). IBD has a high recurrence rate and is so difficult to cure to the extent that the World Health. Organization has classified it as one of the modern intractable diseases (Jackson and De Cruz, 2019). T-cell-mediated inflammation is important in experimental colitis and human IBD (Strober et al, 2007; Zundler and Neurath, 2017)
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