Ion transport mechanisms for smoke inhalation-injured airway epithelial barrier.
Ion transport mechanisms for smoke inhalation-injured airway epithelial barrier.
复制标题
烟雾吸入损伤气道上皮屏障的离子传输机制
DOI：
10.1007/s10565-020-09545-1
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发表时间：
2020-12
影响因子：
6.1
通讯作者：
Ji HL
中科院分区：
文献类型：
--
作者：
Chang J;Chen Z;Zhao R;Nie HG;Ji HL
Smoke inhalation injury is the leading cause of death in firefighters and victims. Inhaled hot air and toxic smoke are the predominant hazards to the respiratory epithelium. We aimed to analyze the effects of thermal stress and smoke aldehyde on the permeability of the airway epithelial barrier. Transepithelial resistance (RTE) and short-circuit current (ISC) of mouse tracheal epithelial monolayers were digitized by an Ussing chamber setup. Zonula occludens-1 tight junctions were visualized under confocal microscopy. A cell viability test and fluorescein isothiocyanate-dextran assay were performed. Thermal stress (40 °C) decreasedRTEin a two-phase manner. Meanwhile, thermal stress increasedISCfollowed by its decline. Na+depletion, amiloride (an inhibitor for epithelial Na+channels [ENaCs]), ouabain (a blocker for Na+/K+-ATPase), and CFTRinh-172 (a blocker of cystic fibrosis transmembrane regulator [CFTR]) altered the responses ofRTEandISCto thermal stress. Steady-state 40 °C increased activity of ENaCs, Na+/K+-ATPase, and CFTR. Acrolein, one of the main oxidative unsaturated aldehydes in fire smoke, eliminatedRTEandISC. Na+depletion, amiloride, ouabain, and CFTRinh-172 suppressed acrolein-sensitiveISC, but showed activating effects on acrolein-sensitiveRTE. Thermal stress or acrolein disrupted zonula occludens-1 tight junctions, increased fluorescein isothiocyanate-dextran permeability but did not cause cell death or detachment. The synergistic effects of thermal stress and acrolein exacerbated the damage to monolayers. In conclusion, the paracellular pathway mediated by the tight junctions and the transcellular pathway mediated by active and passive ion transport pathways contribute to impairment of the airway epithelial barrier caused by thermal stress and acrolein.Graphical abstractThermal stress and acrolein are two essential determinants for smoke inhalation injury, impairing airway epithelial barrier.Transcellular ion transport pathways via the ENaC, CFTR, and Na/K-ATPase are interrupted by both thermal stress and acrolein, one of the most potent smoke toxins.Heat and acrolein damage the integrity of the airway epithelium through suppressing and relocating the tight junctions.
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影响因子：
10.4
作者：
Alwis KU;deCastro BR;Morrow JC;Blount BC
通讯作者：
Blount BC
影响因子：
8.3
作者：
Kis, Adrian;Krick, Stefanie;Salathe, Matthias
通讯作者：
Salathe, Matthias
DOI：
10.1152/ajplung.00126.2014
发表时间：
2014-10-15
影响因子：
4.9
作者：
Chen, Zaixing;Zhao, Runzhen;Ji, Hong-Long
通讯作者：
Ji, Hong-Long
影响因子：
3.3
作者：
HALES, CA;BARKIN, PW;BURKE, J
通讯作者：
BURKE, J
影响因子：
4.6
作者：
Cui Y;Li H;Wu S;Zhao R;Du D;Ding Y;Nie H;Ji HL
通讯作者：
Ji HL