Clostridium butyricum promotes intestinal motility by regulation of TLR2 in interstitial cells of Cajal

S.-J. Sui, Z.-B. Tian, Q.-C. Wang, R. Chen, J. Nie, J.-S. Li, L.-Z. Wei

Department of GI Medicine, The Affiliated Hospital of Qingdao University, Qingdao, China. lzwei82@126.com

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• Pharmacology

OBJECTIVE: Clostridium butyricum (C. butyricum) as a probiotic has been reported to have an important role in the pathogenesis of gastrointestinal diseases. However, the effects of C. butyricum on regulation of intestinal motility of ulcerative colitis (UC) remain unclear. Our study aimed to explore the cross-regulation effect of C. butyricum and toll-like receptor 2 (TLR-2) on UC.

MATERIALS AND METHODS: Interstitial cells of Cajal (ICCs) were treated by C. butyricum for 2 h, the mRNA and protein levels of TLR-2, IL-6, and IL-8 were detected by RT-qPCR and Western blot. Then, TLR2-specific small interfering RNA (si-TLR2) was transfected into ICCs, and the relative expressions of IL-6 and IL-8, SCF, cell viability, ghrelin, SP, and ET were measured by RT-qPCR, Western blot, CCK-8, and ELISA. Besides, the signal pathways of NF-κB and JNK were determined by Western blot.

RESULTS: C. butyricum significantly increased TLR2, IL-6, and IL-8 expressions in ICCs. However, TLR2 silence alleviated C. butyricum-induced IL-6 and IL-8 expressions. Moreover, TLR2 silence significantly inhibited C. butyricum-induced cell viability in ICCs. Additionally, C. butyricum significantly increased SCF expression and promoted the secretion of ghrelin and SP. However, a significant reduction in the levels of SCF, ghrelin, and SP was evident in the silence of TLR2 expression. Besides, TLR2 silence reduced C. butyricum-activation NF-κB and JNK signal pathways in ICCs.

CONCLUSIONS: These findings revealed that C. butyricum promoted intestinal motility by regulation of TLR2 in ICCs, which contributed to understand the molecular mechanisms of C. butyricum on UC.

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