Polydatin attenuates Mycoplasma gallisepticum (HS strain)-induced inflammation injury via inhibiting the TLR6/ MyD88/NF-κB pathway

Microb Pathog. 2020 Dec:149:104552. doi: 10.1016/j.micpath.2020.104552. Epub 2020 Sep 30.

Abstract

Mycoplasma gallisepticum (MG) infection is the main cause of chronic respiratory disease (CRD) characterized by severe respiratory inflammation in chickens. Polydatin (PD) is a resveratrol glycoside isolated from Polygonum cuspidatum, which has prominent anti-inflammatory effect. The purpose of this study was to investigate the therapeutic effect of PD against MG-induced inflammation in chicken and its underlying mechanism. Histopathological analysis showed that PD treatment (15, 30, and 45 mg/kg) apparently alleviated MG-induced pathological changes of chicken embryonic lung. In chicken embryo fibroblast (DF-1) cells, PD treatment (15, 30, and 60 μg/mL) could effectively suppress MG propagation, promote MG-infected cell proliferation and cell cycle progress, and inhibit MG-induced cell apoptosis. ELISA and qPCR assays showed that PD treatment significantly suppressed the expression of interleukin-6 (IL-6), IL-1β and tumor necrosis factor-α (TNF-α) induced by MG both in vivo and in vitro. Besides, molecular studies indicated that the MG-induced levels of toll-like receptor-6 TLR6, myeloid differentiation-88 (MyD88) and nuclear factor κB (NF-κB) were significantly decreased by PD treatment. Moreover, immunofluorescence analysis showed that PD treatment restrained the MG-induced NF-κB-p65 nuclear translocation. Taken together, these results indicate the protective effects of PD against MG-induced inflammation injury in chicken were mainly by inhibiting the TLR6/MyD88/NF-κB pathway.

Keywords: Chicken; Inflammation; Mycoplasma gallisepticum (HS strain); Polydatin; TLR6/MyD88/NF-κB pathway.

MeSH terms

  • Animals
  • Chick Embryo
  • Chickens / metabolism
  • Glucosides
  • Inflammation / drug therapy
  • Mycoplasma gallisepticum* / metabolism
  • Myeloid Differentiation Factor 88 / metabolism
  • NF-kappa B / metabolism
  • Stilbenes
  • Toll-Like Receptor 6 / metabolism
  • Tumor Necrosis Factor-alpha

Substances

  • Glucosides
  • Myeloid Differentiation Factor 88
  • NF-kappa B
  • Stilbenes
  • Toll-Like Receptor 6
  • Tumor Necrosis Factor-alpha
  • polydatin