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.