4.7 Article

Cathelicidin-BF suppresses intestinal inflammation by inhibiting the nuclear factor-κB signaling pathway and enhancing the phagocytosis of immune cells via STAT-1 in weanling piglets

期刊

INTERNATIONAL IMMUNOPHARMACOLOGY
卷 28, 期 1, 页码 61-69

出版社

ELSEVIER
DOI: 10.1016/j.intimp.2015.05.034

关键词

Cathelicidin-BF; Inflammation; Weaning stress; Nuclear factor-kappa B; Phagocytosis; STAT-1

资金

  1. National Science Fund for Distinguished Young Scholars of China [31025027]
  2. Modern Agro-Industry Technology Research System, China [CARS-36]

向作者/读者索取更多资源

The severity of intestinal inflammation in mammals can be profoundly impacted by weaning stress. Cathelicidins protect intestinal homeostasis by not only directly killing bacteria but also immune regulators. Here, we investigated the effects of cathelicidin-BF (C-BF) derived from the snake venoms of Bungarus fasciatus on weaning stress and intestinal inflammation and examined the mechanisms by which C-BF modulates intestinal immune responses in weanling piglets. We found that C-BF treatment significantly increased performance and reduced the diarrheal index in weanling piglets. Serum IL-6, IL-22 and TNF-alpha production was decreased by C-BF treatment We demonstrated that C-BF inhibited the expression of the inflammatory cytokines TNF-alpha, IL-6 and IL-8 but increased the expression of the anti-inflammatory cytokine IL-10 in the intestine. We also demonstrated that C-BF suppressed inflammation by down-regulating the nuclear factor-kappa B (NF-kappa B) signaling pathway in the intestine and in LPS-induced macrophages in vitro. However, C-BF significantly induced the phosphorylation of signal transducer and activator of transcription 1 (STAT-1) to enhance the phagocytosis of macrophages when inflammation was suppressed. In summary, our study demonstrated that C-BF suppressed intestinal inflammation by down-regulating the NF-kappa B signaling pathway and enhancing the phagocytosis of immune cells by activating STAT-1 during weaning. (C) 2015 Published by Elsevier B.V.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.7
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据