Abstract
Immune memory has a protective effect on the human body, but abnormal immune memory is closely related to the occurrence and development of autoimmune diseases including inflammatory bowel disease (IBD). Sishen Pill (SSP) is a classic prescription of traditional Chinese medicine, which is often used to treat chronic colitis, but it is not clear whether SSP can alleviate experimental colitis by remodeling immune memory. In the present study, the therapeutic effect of SSP on chronic colitis induced by dextran sulfate sodium (DSS) was evaluated by colonic length, colonic weight index, macroscopic and microscopic scores, and pathological observation. The cytokine levels were tested by enzyme-linked immunosorbent assay (ELISA); the percentages of central memory T (Tcm) and effector memory T (Tem) cells were analyze\\d by flow cytometry; and activation of phosphoinositide 3-kinase (PI3K)/Akt signaling proteins was measured by western blotting. After 7-days' treatment, SSP alleviated DSS-induced colitis, which was demonstrated by decreased colonic weight index, colonic weight, histopathological injury scores, restored colonic length, gradual recovery of colonic mucosa, and lower levels of interleukin (IL)-2, IL-7, IL-12, and IL-15, while SSP increased IL-10 expression. SSP obviously regulated the quantity and subpopulation of Tcm and Tem cells. Furthermore, SSP markedly inhibited activation of PI3K, Akt, phospho-Akt, Id2, T-bet, forkhead box O3a, Noxa, and C-myc proteins in the PI3K/Akt signaling pathway and activated Rictor, Raptor, tuberous sclerosis complex (TSC)1, TSC2, phospho-AMP-activated kinase (AMPK)-α, AMPK-α, eukaryotic translation initiation factor 4E-binding protein 2, kinesin family member 2a, and 70-kDa ribosomal protein S6 kinase. These results indicate that SSP effectively controls Tem cells in the peripheral blood to relieve experimental colitis induced by DSS, which were potentially related with inhibiting the PI3K/Akt signaling pathway.
Highlights
Inflammatory bowel disease (IBD) is an immune-mediated chronic nonspecific intestinal inflammatory disease, including ulcerative colitis (UC) and Crohn's disease (CD), with the characteristics of alternating remission and recurrence (Xavier and Podolsky, 2007)
There is no direct evidence that SSP treats inflammatory bowel disease (IBD) by regulating immune memory, we found that SSP relieved experimental colitis by inhibiting the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway and regulating the balance between proinflammatory and anti-inflammatory cytokines (Liu et al, 2012; Zhao et al, 2013; Liu et al, 2015)
These results indicated that SSP effectively ameliorated DSSinduced colitis
Summary
Inflammatory bowel disease (IBD) is an immune-mediated chronic nonspecific intestinal inflammatory disease, including ulcerative colitis (UC) and Crohn's disease (CD), with the characteristics of alternating remission and recurrence (Xavier and Podolsky, 2007). N IBD, memory T cells are intermittently reactivated in secondary lymphoid organs and thereafter return to inflammatory tissues (Rosen et al, 2003). Fujii et al (2006) have found that FTY720 inhibits the level of CD4+ Tem and CD4+ Tcm cells to prevent the development of colitis induced by the adoptive transfer of lamina propria (LP) colitogenic CD4+ Tem cells. These studies have indicated potential and effective tactics to prevent the onset and development of autoimmune diseases, including IBD by regulating the function and status of memory T cells
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