肺炎支原体诱导哮喘患者气道上皮细胞表达MUC5AC
2008/04/30
研究证实，感染和粘液素过度分泌都参与了哮喘的急性发作，作者假定肺炎支原体能诱导气道上皮细胞MUC5AC（主要的气道粘液素）的表达，而发挥协同作用。
为了验证这一假说，Kraft等对11例哮喘患者和6例健康志愿者进行支气管镜检查和气道刷检。收集气道上皮细胞并在有/无肺炎支原体的气-液交界培养基中培养并孵育48小时，加入或不加入NF- B和TLR2抑制剂观察反应。定量PCR测定MUC5AC和TLR2 mRNA，ELISA法测定MUC5AC和总蛋白。
研究结果显示：哮喘患者气道上皮细胞在加入肺炎支原体48小时后，MUC5AC mRNA和蛋白的表达显著增加，但健康志愿者上皮细胞的MUC5AC mRNA和蛋白并无相似变化，与不加入肺炎支原体的细胞相当。哮喘患者的气道上皮细胞加入肺炎支原体4小时后，TLR2 mRNA的表达较不加入肺炎支原体的对照组显著增加，NF- B和TLR2抑制剂能显著降低MUC5AC的表达。
作者认为，接触肺炎支原体能显著增加哮喘患者气道上皮细胞MUC5AC mRNA和蛋白的表达，TLR2信号通路可能参与了这一过程。
（韩伟 青岛大学附属青岛市立医院东院呼吸科 266071 摘译）
(Eur Respir J 2008; 31:43-46 )
Eur Respir J 2008; 31:43-46
Mycoplasma pneumoniae induces airway epithelial cell expression of MUC5AC in asthma
M. Kraft, K. B. Adler, J. L. Ingram1,
As excess mucin expression can contribute to the exacerbation of asthma, the present authors hypothesised that Mycoplasma pneumoniae significantly induces MUC5AC (the major airway mucin) expression in airway epithelial cells isolated directly from asthmatic subjects.
A total of 11 subjects with asthma and six normal controls underwent bronchoscopy with airway brushing. Epithelial cells were cultured at an air–liquid interface and incubated with and without M. pneumoniae for 48 h, and in the presence and absence of nuclear factor (NF)- B and a toll-like receptor (TLR)2 inhibitor. Quantitative PCR was performed for MUC5AC and TLR2 mRNA. MUC5AC protein and total protein were determined by ELISA.
M. pneumoniae exposure significantly increased MUC5AC mRNA and protein expression after 48 h in epithelial cells isolated from asthmatic, but not from normal control subjects, at all concentrations as compared to unexposed cells. TLR2 mRNA expression was significantly increased in asthmatic epithelial cells at 4 h compared with unexposed cells. NF- B and TLR2 inhibition reduced MUC5AC expression to the level of the unexposed control in both groups.
Mycoplasma pneumoniae exposure significantly increased MUC5AC mRNA and protein expression preferentially in airway epithelial cells isolated from asthmatic subjects. The toll-like receptor 2 pathway may be involved in this process.
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妊娠期暴露于颗粒会增加新生婴儿哮喘的敏感性
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哮喘患者运动诱发的支气管痉挛对皮质激素的反应以及痰中嗜酸细胞的相关研究
