MicroRNA-155 regulates lipopolysaccharide-induced mucin 5AC overproduction via a suppressor of cytokine signaling 1-mediated mechanism in human bronchial epithelial cells

Respir Physiol Neurobiol. 2019 Jun:264:12-18. doi: 10.1016/j.resp.2019.03.008. Epub 2019 Mar 21.

Abstract

Chronic inflammatory lung diseases accompanied by Gram-negative bacteria infection are characterized by excessive mucin production. Lipopolysaccharide (LPS), the major endotoxin released from Gram-negative bacteria, is a potent inflammatory agonist for mucin overproduction. In this study, we sought to examine whether the toll-like receptor (TLR)-responsive microRNA miR-155 plays a role in LPS-provoked induction of mucin 5AC (MUC5AC) and the potential role of suppressor of cytokine signaling 1 (SOCS1) involved in this process. We found that LPS increased the expression of MUC5AC in association with TLR4-dependent miR-155 induction. The suppression of miR-155 by antagomir led to an excessive production of SOCS1, thereby downregulation of MUC5AC production. Collectively, these data imply that miR-155 is involved in LPS-induced MUC5AC overproduction through a TLR4-dependent manner and thereby the downregulation of SOCS1.

Keywords: Lipopolysaccharide; MicroRNA-155; Mucin 5AC; Suppressor of cytokine signaling 1; Toll-like receptor 4.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Bronchi / metabolism*
  • Cell Line
  • Down-Regulation
  • Epithelial Cells / metabolism*
  • Humans
  • Lipopolysaccharides / metabolism*
  • MicroRNAs / metabolism*
  • Mucin 5AC / metabolism*
  • Suppressor of Cytokine Signaling 1 Protein / metabolism*
  • Toll-Like Receptor 4 / metabolism*
  • Up-Regulation

Substances

  • Lipopolysaccharides
  • MIRN155 microRNA, human
  • MUC5AC protein, human
  • MicroRNAs
  • Mucin 5AC
  • SOCS1 protein, human
  • Suppressor of Cytokine Signaling 1 Protein
  • TLR4 protein, human
  • Toll-Like Receptor 4