Protective effect of chlorogenic acid on lipopolysaccharide-induced inflammatory response in dairy mammary epithelial cells

Microb Pathog. 2018 Nov:124:178-182. doi: 10.1016/j.micpath.2018.07.030. Epub 2018 Jul 24.

Abstract

Mastitis is a major disease of dairy cattle. Given the recent emergence of antibiotics resistance to mastitis, new intramammary treatments are urgently required. In the present study, we investigated whether lipopolysaccharide (LPS) could induce the increase in the proinflammatory cytokines in bovine mammary epithelial cells (MECs), and whether a natural antimicrobial compound Chlorogenic acid (CGA) could attenuate the inflammatory responses induced by LPS and thus could be a potential therapeutic compound for bovine mastitis. Our results indicated that LPS could induce the expression of proinflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukine (IL)-1β and IL-6, and the activation of NF-κB p65 and p-p65 in primary bovine MECs. Furthermore, CGA significantly inhibited not only the protein expression of NF-κB p65 and p-p65 but also the mRNA expression of TNF-α, IL-1β and IL-6 after LPS treatment in primary bovine MECs. These results suggested that CGA had anti-inflammatory role by inhibiting NF-κB activation. In conclusion, CGA could be possibly used as a potential therapeutic compound for bovine mastitis.

Keywords: Bovine mastitis; Chlorogenic acid; Mammary epithelial cell; Proinflammatory cytokines.

MeSH terms

  • Animals
  • Cattle
  • Chlorogenic Acid / administration & dosage*
  • Epithelial Cells / drug effects*
  • Epithelial Cells / immunology
  • Female
  • Interleukin-1beta / genetics
  • Interleukin-1beta / immunology
  • Lipopolysaccharides / adverse effects*
  • Mammary Glands, Animal / drug effects*
  • Mammary Glands, Animal / immunology
  • Mastitis, Bovine / drug therapy*
  • Mastitis, Bovine / genetics
  • Mastitis, Bovine / immunology
  • Toll-Like Receptor 4 / genetics
  • Toll-Like Receptor 4 / immunology
  • Transcription Factor RelA / genetics
  • Transcription Factor RelA / immunology
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / immunology

Substances

  • Interleukin-1beta
  • Lipopolysaccharides
  • Toll-Like Receptor 4
  • Transcription Factor RelA
  • Tumor Necrosis Factor-alpha
  • Chlorogenic Acid