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

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

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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