Hyperoside inhibits proinflammatory cytokines in human lung epithelial cells infected with Mycoplasma pneumoniae

Mol Cell Biochem. 2019 Mar;453(1-2):179-186. doi: 10.1007/s11010-018-3443-4. Epub 2018 Oct 22.

Abstract

Mycoplasma pneumoniae pneumonia (MPP) is the most common respiratory infection in young children and its incidence has increased worldwide. In this study, high expression of chemokine ligand 5 (CCL5) was observed in the serum of MPP patients, and its expression was positively correlated to DNA of M. pneumoniae (MP-DNA). In vitro, M. pneumoniae (MP) infection to A549 cells induced the expression of CCL5, chemokines receptor 4 (CCR4), nuclear factor-κB (NF-κB) nuclear protein, and phosphorylation of NF-κB-p65 (p-NF-κB-p65), whereas NF-κB cytoplasmic protein was decreased. On the contrary, treatment of hyperoside counteracted the induction of MP infection and promoted the proliferation of MP-infected A549 cells. Similarly, MP-induced IL-8 and TNF-α production was also markedly reduced by hyperoside. And CCR4 inhibitor AZD2098 had a better effect than hyperoside. In addition, CCL5 recombinant protein inhibited the effect of hyperoside to promote IL-8 and TNF-α production and CCR4 expression. These results indicated that CCL5 may be involved in the progression of MPP, and hyperoside was beneficial for MPP probably through CCL5-CCR4 interactions, which may provide a potential effective therapy for MPP.

Keywords: AZD2098; CCL5–CCR4; Hyperoside; Mycoplasma pneumoniae pneumonia; NF-κB.

MeSH terms

  • A549 Cells
  • Chemokine CCL5 / metabolism
  • Chemokine CCL8 / metabolism
  • Epithelial Cells* / metabolism
  • Epithelial Cells* / microbiology
  • Epithelial Cells* / pathology
  • Humans
  • Mycoplasma pneumoniae / metabolism*
  • Pneumonia, Mycoplasma* / drug therapy
  • Pneumonia, Mycoplasma* / metabolism
  • Pneumonia, Mycoplasma* / pathology
  • Quercetin / analogs & derivatives*
  • Quercetin / pharmacology
  • Respiratory Mucosa* / metabolism
  • Respiratory Mucosa* / microbiology
  • Respiratory Mucosa* / pathology
  • Transcription Factor RelA / metabolism
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • CCL5 protein, human
  • CCL8 protein, human
  • Chemokine CCL5
  • Chemokine CCL8
  • RELA protein, human
  • Transcription Factor RelA
  • Tumor Necrosis Factor-alpha
  • hyperoside
  • Quercetin