Lipopolysaccharides induces MUC5AC overproduction in human nasal epithelium
Lipopolysaccharides induces MUC5AC overproduction in human nasal epithelium
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DOI：
10.1007/s00405-012-2037-0
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发表时间：
2013-02-01
影响因子：
2.6
通讯作者：
Wan, Lingyan
中科院分区：
文献类型：
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作者：
Wang, Weiwei;Xu, Xianyan;Wan, Lingyan
鼻上皮粘液蛋白分泌过多是鼻炎性疾病的一个重要特征。我们研究了脂多糖（LPS）参与人鼻上皮细胞MUC5AC亚型表达的机制。体外培养原代人鼻上皮细胞，LPS （10 nM/ml或1 μ M/ml）作用12和24 h，测定LPS诱导的鼻上皮细胞MUC5AC蛋白水平。检测核因子κ Bp65 （nf - κ Bp65）及其抑制剂κ B α (I κ B α)蛋白表达水平，实时荧光定量PCR检测白细胞介素-1 β (IL-1 β) mRNA表达水平。LPS上调人鼻上皮细胞MUC5AC蛋白，我们确定MUC5AC表达上调是由于I κ B α蛋白的时间和剂量依赖性降解，导致nf - κ Bp65核易位增加。随后，我们还确定LPS可以以时间和剂量依赖的方式诱导IL-1 β mRNA。这些数据表明，LPS处理通过促进I kappa B α的降解和NF-kappa Bp65的核定位来激活NF-kappa B，从而诱导MUC5AC过量产生。
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.