Lipopolysaccharides induces MUC5AC overproduction in human nasal epithelium

Eur Arch Otorhinolaryngol. 2013 Feb;270(2):541-7. doi: 10.1007/s00405-012-2037-0. Epub 2012 May 11.

Abstract

Hyperproduction of mucin in the nasal epithelium is an important feature of nasal inflammatory diseases. We investigated the mechanism of lipopolysaccharides (LPS) involvement in mucin 5 subtype AC (MUC5AC) expression in human nasal epithelial cells. The primary human nasal epithelial cells were cultured in vitro, which were treated with LPS (10 nM/ml or 1 μM/ml) for 12 and 24 h. LPS-induced MUC5AC protein was determined in nasal epithelial cells. The levels of nuclear factor kappa B p65 (NF-κBp65) and its inhibitor kappa Bα (IκBα) protein were also detected, and interleukin-1β (IL-1β) mRNA was detected by real-time PCR. LPS up-regulated MUC5AC protein in human nasal epithelial cells, and we determined that the up-regulation of MUC5AC expression was due to a time- and dose-dependent degradation of IκBα protein, which resulted in the increase of NF-κBp65 nuclear translocation. Subsequently, we also determined that LPS can induce IL-1β mRNA in a time- and dose-dependent manner. These data show that LPS treatment activated NF-κB by promoting the degradation of IκBα and the nuclear localization of NF-κBp65, which induced MUC5AC overproduction.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Blotting, Western
  • Cells, Cultured
  • Humans
  • Immunohistochemistry
  • Interleukin-1beta / metabolism
  • Lipopolysaccharides / pharmacology*
  • Middle Aged
  • Mucin 5AC / metabolism*
  • NF-kappa B / metabolism
  • Nasal Mucosa / metabolism*
  • Young Adult

Substances

  • Interleukin-1beta
  • Lipopolysaccharides
  • Mucin 5AC
  • NF-kappa B