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首页> 外文期刊>Life sciences >Metabolic activation of A549 human airway epithelial cells by organic dust: A study based on microphysiometry.
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Metabolic activation of A549 human airway epithelial cells by organic dust: A study based on microphysiometry.

机译：有机尘埃对A549人气道上皮细胞的代谢活化：基于微生理学的研究。

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A Cytosensor microphysiometer, which measures extracellular acidification rate (ECAR), was used to study the early metabolic activation by organic dust from a swine confinement building in a human airway epithelial cell line, A549. The dust is known to cause an intense airway inflammatory reaction following inhalation in vivo and cytokine release in vitro. Dimethyl amiloride (DMA) was used to study sodium/proton exchanger (NHE) activity in cells growing at different cell densities. Exposing cells at low density to dust induced an initial release of acid not involving NHE, followed by a sustained DMA-sensitive NHE activation. In cells near high density, NHE was not activated during exposure resulting in a modest increase in ECAR. Exposing cells at high density resulted in a bi-phasic ECAR pattern; an initial increase in proton release followed by an inhibition of ECAR below baseline. Pretreatment with pertussis toxin (PTX), an inhibitor of receptor/G(ialpha)-coupled signal transductions did not affect ECAR in low and medium density cells, but abolished the inhibition of ECAR in high-density cells. The dust did not prevent forskolin-induced cAMP accumulation and PTX did not affect cAMP in near-confluent cells suggesting the PTX-effect to be cAMP-independent. The ECAR response to organic dust was similar to that of lipopolysaccharide (LPS) except for high-density cells where PTX did not influence the LPS-induced decrease in ECAR below baseline. In summary, the organic dust induces PTX-sensitive (cAMP independent) signalling in near-confluent A549 epithelial cells and, depending on cell density opposing effects on NHE activity during exposure.
机译：一种用于测量细胞外酸化率（ECAR）的细胞传感器微生理仪被用于研究人类气道上皮细胞系A549中猪禁闭建筑物中有机尘埃引起的早期代谢活化。已知粉尘会在体内吸入并在体外释放细胞因子后引起强烈的气道炎症反应。二甲基阿米洛利（DMA）用于研究在不同细胞密度下生长的细胞中的钠/质子交换剂（NHE）活性。将细胞以低密度暴露于灰尘下会诱导不涉及NHE的酸的初始释放，然后持续进行DMA敏感的NHE活化。在接近高密度的细胞中，暴露期间NHE未被激活，导致ECAR适度增加。高密度暴露细胞会导致两相ECAR模式。最初质子释放增加，随后将ECAR抑制到基线以下。百日咳毒素（PTX）的预处理是一种受体/ G（ialpha）偶联的信号转导抑制剂，在中低密度细胞中不影响ECAR，但取消了对高密度细胞中ECAR的抑制作用。灰尘并不能阻止毛喉素诱导的cAMP积累，PTX不会影响近汇合细胞中的cAMP，这表明PTX效应是不依赖cAMP的。 ECAR对有机粉尘的响应与脂多糖（LPS）相似，除了高密度细胞（其中PTX不会影响LPS诱导的ECAR降低至基线以下）。总而言之，有机尘埃会在接近汇合的A549上皮细胞中诱导PTX敏感（独立于cAMP），并取决于暴露期间对NHE活性产生相反作用的细胞密度。

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