Chitosan oligosaccharide-mediated attenuation of LPS-induced inflammation in IPEC-J2 cells is related to the TLR4/NF-κB signaling pathway

  • Carbohydr Polym. 2019 Sep 1;219:269-279. doi: 10.1016/j.carbpol.2019.05.036.
Lin Shi  1 ,  Biao Fang  2 ,  Yanhong Yong  3 ,  Xuewen Li  3 ,  Dongliang Gong  3 ,  Junyu Li  2 ,  Tianyue Yu  2 ,  Ravi Gooneratne  4 ,  Zhenhua Gao  5 ,  Sidong Li  6 ,  Xianghong Ju  7
Affiliations
  • 1. Department of Animal Science, College of Agricultural Sciences, Guangdong Ocean University, Zhanjiang, Guangdong, 524088, China; Shenzhen Institute of Guangdong Ocean University, Shenzhen, 518018, China.
  • 2. Department of Animal Science, College of Agricultural Sciences, Guangdong Ocean University, Zhanjiang, Guangdong, 524088, China.
  • 3. Department of Veterinary Medicine, College of Agricultural Sciences, Guangdong Ocean University, Zhanjiang, Guangdong, 524088, China.
  • 4. Department of Wine, Food and Molecular Biosciences, Faculty of Agriculture and Life Sciences, Lincoln University, Lincoln 7647, New Zealand.
  • 5. Department of Animal Science, College of Agricultural Sciences, Guangdong Ocean University, Zhanjiang, Guangdong, 524088, China. Electronic address: [email protected].
  • 6. College of Chemistry and Environment, Guangdong Ocean University, Zhanjiang, Guangdong, 524088, China. Electronic address: [email protected].
  • 7. Department of Veterinary Medicine, College of Agricultural Sciences, Guangdong Ocean University, Zhanjiang, Guangdong, 524088, China; Shenzhen Institute of Guangdong Ocean University, Shenzhen, 518018, China. Electronic address: [email protected].
PMID: 31151525 DOI: 10.1016/j.carbpol.2019.05.036
Abstract

The protective mechanism of chitosan oligosaccharide (COS) against lipopolysaccharides (LPS) -induced inflammatory responses in IPEC-J2 and in mice with DSS dextran sulfate sodium (DSS) -induced colitis is reported. Upon exposure to LPS, the proliferation rate of IPEC-J2 cells markedly decreased, and epithelial cell integrity was compromised. However, COS pretreatment significantly reduced these changes. Low-concentration (200 μg/mL) COS up-regulated Toll-like Receptor 4 (TLR4) and nuclear p65 expression, but inhibited LPS-induced expression of nuclear p65, IL-6, and IL-8. Addition of the TLR4 Inhibitor reduced nuclear p65, IL-6, and IL-8 expression in IPEC-J2 cells exposed to COS or LPS alone, and a slight up-regulation in nuclear p65 was observed in COS and LPS co-treated cells. Medium-dose COS (600 mg/kg/d) protected against DSS-induced colitis, in which TLR4 and nuclear p65 expression levels were decreased. We postulate that the prevention of both LPS- and DSS -induced inflammatory responses in IPEC-J2 cells and mice by COS are related to the inhibition of the TLR4/NF-κB signaling pathway.

Keywords
Chitosan oligosaccharide (COS); IPEC-J2; Inflammation; TLR4/NF-κB.
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