Epithelial permeability, inflammation, and oxidant stress in the air spaces of smokers

Epithelial permeability, inflammation, and oxidant stress in the air spaces of smokers
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DOI:
10.1164/ajrccm.159.2.9804080
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发表时间:
1999-02-01
影响因子:
24.7
通讯作者:
MacNee, W
MacNee, W
中科院分区:
医学1区
文献类型:
--
作者:
Morrison, D;Rahman, I;MacNee, W

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导致吸烟者空气空间渗透性增加的机制尚不清楚。本研究的目的是评估吸烟对吸烟者气道上皮通透性、炎症和氧化应激的急性和慢性影响。14名吸烟者在戒烟12 h(慢性吸烟)和吸两支烟1 h(急性吸烟)后进行了Tc-99 m-DTPA肺扫描。每名吸烟者在慢性(n = 8)或急性吸烟(n = 7)后还接受了支气管镜检查和支气管肺泡灌洗(BAL)。7名非吸烟者也接受了支气管镜检查和BAL。长期吸烟后,Tc-99 m-DTPA清除50%的时间(t(50))为16.7 ± 1.3 min(平均值± SE),急性吸烟后进一步缩短至14.8 ± 1.0 min(p < 0.01)。急性吸烟组支气管肺泡灌洗液(BALF)中神经细胞数较非吸烟组明显增多(P < 0.05)。慢性(p < 0.01)和急性(p < 0.001)吸烟后,混合BAL白细胞的超氧化物释放增加,硫代巴比妥酸反应物质(TBARS)也增加,这提供了血浆脂质过氧化的证据(慢性,p < 0.05;急性,p < 0.05)。两个吸烟组血浆中Trolox等效抗氧化能力(TEAC)降低(p < 0.001),BALF中Trolox等效抗氧化能力(TEAC)升高(p < 0.05)。因此,该研究表明,吸烟者的上皮通透性急剧增加,空气中嗜中性粒细胞数量增加,伴随着氧化应激增加的证据。
The mechanism responsible for the increased air-space permeability in cigarette smokers is unknown. The aim of this study was to assess the acute and chronic effects of cigarette smoking on epithelial permeability, inflammation, and oxidant stress in the air spaces of smokers. Fourteen cigarette smokers underwent Tc-99m-diethylenetriamine pentaacetic acid (Tc-99m-DTPA) lung scans after abstaining from smoking for 12 h (chronic smoking) and 1 h after smoking two cigarettes (acute smoking). Each smoker also underwent bronchoscopy and bronchoalveolar lavage (BAL) after either chronic (n = 8) or acute smoking (n = 7). Seven nonsmokers also underwent bronchoscopy and BAL. The time to 50% clearance of Tc-99m-DTPA (t(50)) after chronic smoking was 16.7 +/- 1.3 min (mean +/- SE), and was further reduced after acute smoking to 14.8 +/- 1.0 min (p < 0.01). Neutrophil numbers were increased in bronchoalveolar lavage fluid (BALF) in the acute smoking group as compared with the nonsmokers (p < 0.05). Superoxide release from mixed BAL leukocytes was increased after chronic (p < 0.01) and acute (p < 0.001) smoking, as were thiobarbituric acid-reactive species (TBARS), providing evidence of lipid peroxidation in plasma (chronic, p < 0.05; acute, p < 0.05). Trolox equivalent antioxidant capacity (TEAC) was reduced in plasma (p < 0.001) and increased in BALF (p < 0.05) in both smoking groups. The study therefore showed an acute increase in epithelial permeability and an increase in the number of neutrophils in the air spaces of cigarette smokers concomitant with evidence of increased oxidant stress.