Journal
INNATE IMMUNITY
Volume 24, Issue 1, Pages 40-46Publisher
SAGE PUBLICATIONS LTD
DOI: 10.1177/1753425917741970
Keywords
Sodium butyrate; intestinal barrier; mast cell; inflammatory mediators; mitogen-activated protein kinases; weaned pigs
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Funding
- National Key R D Program [2016YFD0501210]
- Zhejiang Province Key R D Project [2015C02022]
- Zhejiang Province Major Science and Technology Project [2015C03006]
- Special Fund for Agro-scientific Research in the Public Interest [201403047]
- Dabeinong Funds for Discipline Development and Talent Training in Zhejiang University
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The present study aimed to investigate the effects of sodium butyrate on the intestinal barrier and mast cell activation, as well as inflammatory mediator production, and determine whether mitogen-activated protein kinase signaling pathways are involved in these processes. A total of 72 piglets, weaned at 28 +/- 1 d age, were allotted to two dietary treatments (control vs. 450mg/kg sodium butyrate) for 2 wk. The results showed that supplemental sodium butyrate increased daily gain, improved intestinal morphology, as indicated by greater villus height and villus height:crypt depth ratio, and intestinal barrier function reflected by increased transepithelial electrical resistance and decreased paracellular flux of dextran (4kDa). Moreover, sodium butyrate reduced the percentage of degranulated mast cells and its inflammatory mediator content (histamine, tryptase, TNF- and IL-6) in the jejunum mucosa. Sodium butyrate also decreased the expression of mast cell-specific tryptase, TNF- and IL-6 mRNA. Sodium butyrate significantly decreased the phosphorylated ratio of JNK whereas not affecting the phosphorylated ratios of ERK and p38. The results indicated that the protective effects of sodium butyrate on intestinal integrity were closely related to inhibition of mast cell activation and inflammatory mediator production, and that the JNK signaling pathway was likely involved in this process.
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