Selenium deficiency induced necroptosis, Th1/Th2 imbalance, and inflammatory responses in swine ileum
文献类型: 外文期刊
第一作者: Zhang, Yuan
作者: Zhang, Yuan;Zhang, Ziwei;Zhang, Jiuli;Zhang, Ziwei;Bao, Jun;Tang, Chaohua
作者机构:
关键词: ileum; inflammation; necroptosis; Se-deficient swine; Th1; Th2 balance
期刊名称:JOURNAL OF CELLULAR PHYSIOLOGY ( 影响因子:6.384; 五年影响因子:5.987 )
ISSN: 0021-9541
年卷期:
页码:
收录情况: SCI
摘要: Selenium (Se) deficiency has a significant impact on the swine breeding industry by inducing digestive system damage and diarrhea. However, the molecular mechanism remains unclear. Our objectives were to investigate if different amounts of necroptosis, inflammatory responses, and T helper cell 1/T helper cell 2 (Th1/Th2) imbalances were induced by Se deficiency in intestinal porcine jejunal epithelial cells (IPEC-J2) and swine ileum tissue. Therefore, Se-deficient models were successfully established both in vitro and in vivo. In the current study, the cell morphological observation results showed that Se deficiency seriously affected the growth and differentiation of IPEC-J2 cells. Moreover, the necroptosis staining and histomorphology observation results showed that the number of necroptotic cells increased significantly, and the ileal tissue exhibited abnormal structures, including necroptotic features and inflammatory cell infiltration, in the Se-deficient group. Furthermore, Se deficiency resulted in accelerated cell necroptosis by increasing (p < .05) the expression of genes related to the tumor necrosis factor-alpha pathway at both the protein and messenger RNA (mRNA) levels compared to the control group. Moreover, the relative mRNA and protein expression of the inflammatory genes and their responses to dietary Se deficiency were consistent with the resultant Th1/Th2 imbalances in vitro and in vivo. Taken together, the results suggested that Se deficiency caused necroptosis, inflammatory responses, and abnormal expression of cytokines in swine ileum tissue. These findings might help us to explain the damage induced by Se deficiency to the digestive system of swine.
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