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首页> 外文期刊>Allergy >Human lung mast cells modulate the functions of airway smooth muscle cells in asthma.
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Human lung mast cells modulate the functions of airway smooth muscle cells in asthma.

机译：人肺肥大细胞调节哮喘中气道平滑肌细胞的功能。

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BACKGROUND: Activated mast cell densities are increased on the airway smooth muscle in asthma where they may modulate muscle functions and thus contribute to airway inflammation, remodelling and airflow obstruction. OBJECTIVES: To determine the effects of human lung mast cells on the secretory and proliferative functions of airway smooth muscle cells from donors with and without asthma. METHODS: Freshly isolated human lung mast cells were stimulated with IgE/anti-IgE. Culture supernatants were collected after 2 and 24 h and the mast cells lysed. The supernatants/lysates were added to serum-deprived, subconfluent airway smooth muscle cells for up to 48 h. Released chemokines and extracellular matrix were measured by ELISA, proliferation was quantified by [(3) H]-thymidine incorporation and cell counting, and intracellular signalling by phospho-arrays. RESULTS: Mast cell 2-h supernatants reduced CCL11 and increased CXCL8 and fibronectin production from both asthmatic and nonasthmatic muscle cells. Leupeptin reversed these effects. Mast cell 24-h supernatants and lysates reduced CCL11 release from both muscle cell types but increased CXCL8 release by nonasthmatic cells. The 24-h supernatants also reduced asthmatic, but not nonasthmatic, muscle cell DNA synthesis and asthmatic cell numbers over 5 days through inhibiting extracellular signal-regulated kinase (ERK) and phosphatidylinositol (PI3)-kinase pathways. However, prostaglandins, thromboxanes, IL-4 and IL-13 were not involved in reducing the proliferation. CONCLUSIONS: Mast cell proteases and newly synthesized products differentially modulated the secretory and proliferative functions of airway smooth muscle cells from donors with and without asthma. Thus, mast cells may modulate their own recruitment and airway smooth muscle functions locally in asthma.
机译：背景：哮喘患者气道平滑肌中活化的肥大细胞密度增加，它们可能调节肌肉功能，从而导致气道炎症，重塑和气流阻塞。目的：确定人肺肥大细胞对有或没有哮喘的供体气道平滑肌细胞分泌和增殖功能的影响。方法：用IgE /抗IgE刺激新鲜分离的人肺肥大细胞。 2和24小时后收集培养上清液，并裂解肥大细胞。将上清液/裂解物添加至血清缺乏的，亚汇合的气道平滑肌细胞长达48小时。通过ELISA测量释放的趋化因子和细胞外基质，通过[（3 H）-胸苷掺入和细胞计数，以及通过磷酸阵列的细胞内信号传导，对增殖进行定​​量。结果：肥大细胞2-h上清液减少了哮喘和非哮喘性肌肉细胞的CCL11并增加了CXCL8和纤连蛋白的产生。 Leupeptin逆转了这些作用。肥大细胞的24小时上清液和裂解物减少了两种肌肉细胞的CCL11释放，但非哮喘细胞的CXCL8释放增加。通过抑制细胞外信号调节激酶（ERK）和磷脂酰肌醇（PI3）激酶途径，在24天的上清液中还可以在5天之内减少哮喘但非哮喘的肌肉细胞DNA的合成和哮喘细胞的数量。然而，前列腺素，血栓烷，IL-4和IL-13不参与减少增殖。结论：肥大细胞蛋白酶和新合成的产物差异地调节患有和不患有哮喘的供体的气道平滑肌细胞的分泌和增殖功能。因此，肥大细胞可在哮喘中局部调节其自身的募集和气道平滑肌功能。

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