The Effect of Clostridium butyricum-Derived Lipoteichoic Acid on Lipopolysaccharide-Stimulated Porcine Intestinal Epithelial Cells

文献类型： 外文期刊

第一作者： Chen, Qu

作者： Chen, Qu;Ma, Lingyan;Wen, Yang;Lyu, Wentao;Yu, Minjie;Yang, Hua;Xiao, Yingping

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关键词： Clostridium butyricum; inflammatory factors; IPEC-J2; lipopolysaccharide; lipoteichoic acid

期刊名称：VETERINARY MEDICINE AND SCIENCE （ 影响因子：1.7； 五年影响因子：2.0 ）

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年卷期： 2025 年 11 卷 1 期

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收录情况： SCI

摘要： BackgroundClostridium butyricum is a probiotic widely used in animal husbandry, and there is evidence to suggest that it can alleviate intestinal inflammation in pigs and may be related to its lipoteichoic acid (LTA), but the mechanism is still unclear.ObjectiveThis study aimed to determine the regulatory effect and potential mechanism of C. butyricum LTA on LPS-stimulated inflammation in intestinal porcine epithelial line-J2 (IPEC-J2).MethodsIPEC-J2 cells were treated with LPS and different concentrations of LTA (0.05, 0.1 and 0.15 mM). After treatment of 0.5, 1.5 and 4.5 h, the cell culture media were collected for the measurement of TNF-alpha and IL-10 by using ELISA kits, and the cells were collected for RT-qPCR and Western blotting detections. Further elucidating the pathway of LTA regulating IL-10 and TNF-alpha gene expression by inhibiting key proteins in the toll-like receptor pathway with antagonists C34, PDTC, SB230580 and U0126.ResultsHigh-dose LTA significantly promoted the secretion of the anti-inflammatory factor IL-10 in IPEC-J2 cells, and inhibited the expression and secretion of pro-inflammatory TNF-alpha in the short term. LTA inhibited the gene expression of TLR4 in LPS-stimulated cells and reduced the protein phosphorylation levels of p38, ERK1/2 and p65. The inhibition of TLR4, p38, ERK1/2 and p65 reduced the TNF-alpha gene expression caused by LPS; LTA increased TLR2 gene expression, inhibition of p38, ERK and p65 rather than TLR4 reduced the IL-10 gene expression.ConclusionOur study found that C. butyricum LTA was an important component of C. butyricum regulating the inflammatory response of IPEC-J2 cells. LTA mainly reduced the expression of TNF-alpha by inhibiting TLR4, while stimulating TLR2 increased the expression of IL-10. Downstream p65, p38 and ERK1/2 were involved in regulating both TNF-alpha and IL-10. However, TLR4 was only related to the increase in TNF-alpha caused by LPS and not to the increase in IL-10 caused by LTA. Our work supplemented the probiotic mechanism of C. butyricum and provided a theoretical basis for the application of C. butyricum LTA.

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