Lipopolysaccharides induces MUC5AC overproduction in human nasal epithelium

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 mu M/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-kappa Bp65) and its inhibitor kappa B alpha (I kappa B alpha) protein were also detected, and interleukin-1 beta (IL-1 beta) 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 I kappa B alpha protein, which resulted in the increase of NF-kappa Bp65 nuclear translocation. Subsequently, we also determined that LPS can induce IL-1 beta mRNA in a time- and dose-dependent manner. These data show that LPS treatment activated NF-kappa B by promoting the degradation of I kappa B alpha and the nuclear localization of NF-kappa Bp65, which induced MUC5AC overproduction.