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首页> 外文期刊>American Journal of Physiology >Moraxella catarrhalis induces inflammatory response of bronchial epithelial cells via MAPK and NF-kappaB activation and histone deacetylase activity reduction.
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Moraxella catarrhalis induces inflammatory response of bronchial epithelial cells via MAPK and NF-kappaB activation and histone deacetylase activity reduction.

机译：卡他莫拉氏菌通过MAPK和NF-κB活化以及组蛋白脱乙酰基酶活性降低来诱导支气管上皮细胞的炎症反应。

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摘要

Moraxella catarrhalis is a major cause of infectious exacerbations of chronic obstructive lung disease (COPD) and may also contribute to the pathogenesis of COPD. Little is known about M. catarrhalis-bronchial epithelium interaction. We investigated activation of M. catarrhalis infected bronchial epithelial cells and characterized the signal transduction pathways. Moreover, we tested the hypothesis that the M. catarrhalis-induced cytokine expression is regulated by acetylation of histone residues and controlled by histone deacetylase activity (HDAC). We demonstrated that M. catarrhalis induced a strong time- and dose-dependent inflammatory response in the bronchial epithelial cell line (BEAS-2B), characterized by the release of IL-8 and GM-CSF. For this cytokine liberation activation of the ERK and p38 mitogen-activated protein (MAP) kinases and transcription factor NF-kappaB was required. Furthermore, M. catarrhalis-infected bronchial epithelial cells showed an enhanced acetylation of histone H3 and H4 globally and at the promoter of the il8 gene. Preventing histone deacetylation by the histone deacetylase inhibitor trichostatin A augmented the M. catarrhalis-induced IL-8 response. After exposure to M. catarrhalis, we found a decrease in global histone deacetylase expression and activity. Our findings suggest that M. catarrhalis-induced activation of il8 gene transcription was caused by interference with epigenetic mechanisms regulating il8 gene accessibility. Our findings provide insight into important molecular and cellular mechanisms of M. catarrhalis-induced activation of human bronchial epithelium.
机译：卡他莫拉菌是慢性阻塞性肺疾病（COPD）感染恶化的主要原因，也可能是COPD的发病机理。关于卡他莫拉氏菌-支气管上皮的相互作用知之甚少。我们调查了卡他莫拉菌感染的支气管上皮细胞的激活并表征了信号转导途径。此外，我们测试了假说，卡他莫拉菌诱导的细胞因子表达受组蛋白残基乙酰化的调节，并受组蛋白脱乙酰基酶活性（HDAC）的控制。我们证明卡他氏菌在支气管上皮细胞系（BEAS-2B）中诱导了强烈的时间依赖性和剂量依赖性炎症反应，其特征在于IL-8和GM-CSF的释放。对于这种细胞因子的释放，需要激活ERK和p38丝裂原活化蛋白（MAP）激酶以及转录因子NF-kappaB。此外，粘膜炎莫拉氏菌感染的支气管上皮细胞整体上以及在il18基因的启动子处显示出组蛋白H3和H4的乙酰化增强。通过组蛋白脱乙酰基酶抑制剂曲古抑菌素A防止组蛋白脱乙酰基化可增强卡他莫拉菌诱导的IL-8应答。暴露于粘膜炎莫拉氏菌后，我们发现整体组蛋白脱乙酰基酶表达和活性下降。我们的发现表明，卡他莫拉氏菌诱导的il8基因转录激活是由干扰调节il8基因可及性的表观遗传机制引起的。我们的发现提供了对粘膜炎莫拉氏菌诱导的人支气管上皮激活的重要分子和细胞机制的见解。

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