Abstract
The T follicular helper T (Tfh) cells play a significant role in the pathogenesis of inflammatory bowel disease (IBD), which is regulated by the Bcl-6/Blimp-1 pathway. Some studies have suggested that regulating activation of the Bcl-6/Blimp-1 pathway should be an effective method to treat IBD. Sishen Pill (SSP) has been used frequently to treat chronic colitis. Its mechanism is related to the downstream proteins in the Bcl-6/Blimp-1 pathway. However, it is unknown whether SSP regulates the function and differentiation of Tfh cells to treat IBD. In the present study, chronic colitis was induced by dextran sodium sulfate and treated with SSP for 7 days. SSP effectively treated chronic colitis, regulated the balance between Tfh10, Tfh17 and T follicular regulatory cells, while SSP increased the Blimp-1 level, inhibited expressions of Bcl-6, T-cell costimulator, programmed death (PD)-1 and PD-ligand 1 on the surface of Tfh cells. SSP inhibited activation of BcL-6, phosphorylated signal transducer and activator of transcription (p-STAT)3, signal lymphocyte activation molecule (SLAM)-associated protein but improved Blimp-1 and STAT3 expression in colonic tissues. The results indicated that SSP regulated the differentiation and function of Tfh cells to treat IBD, which was potentially related with inhibiting the Bcl-6/Blimp-1 pathway.
Highlights
Inflammatory bowel diseases (IBDs), including ulcerative colitis (UC) and Crohn’s disease (CD), are characterized by idiopathic chronic intestinal inflammation (Sairenji et al, 2017)
Pathological sections of colonic tissues from colitis mice treated with Sishen Pill (SSP) and 5-aminosalicylic acid (ASA) showed fewer ulcers, decreased inflammatory cell infiltration, and colonic epithelial cell hyperplasia (Figure 1F)
The results showed that SSP ameliorated pathological colonic damage in dextran sulfate sodium (DSS)-induced colitis
Summary
Inflammatory bowel diseases (IBDs), including ulcerative colitis (UC) and Crohn’s disease (CD), are characterized by idiopathic chronic intestinal inflammation (Sairenji et al, 2017). Their pathogenic factors are closely related to the environment, microorganisms, genes, and immunity (Zhang and Li, 2014; Kelsen and Sullivan, 2017). A large number of studies have found that abnormal function and differentiation of T follicular helper (Tfh) cells can lead to autoimmune diseases including IBD (Mesquita et al, 2016; Ueno, 2016). Tfh cell differentiation is mainly divided into three phases (Crotty, 2014). The first phase is early Tfh cell differentiation, which is mainly performed by dendritic cells (DCs)
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