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首页> 外文期刊>Archives of Toxicology >Irritant-induced asthma to hypochlorite in mice due to impairment of the airway barrier
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Irritant-induced asthma to hypochlorite in mice due to impairment of the airway barrier

机译：由于气道屏障的损害，老鼠中枯氯酸盐刺激哮喘

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摘要

Inhalation of commonly present irritants, such as chlorine and chlorine derivatives, can cause adverse respiratory effects, including irritant-induced asthma (IIA). We hypothesize that due to airway barrier impairment, exposure to hypochlorite (ClO-) can result in airway hypersensitivity. C57Bl/6 mice received an intra-peritoneal (i.p.) injection of the airway damaging agent naphthalene (NA, 200 mg/kg body weight) or vehicle (mineral oil, MO). In vivo micro-computed tomography (CT) images of the lungs were acquired before and at regular time points after the i.p. treatment. After a recovery period of 14 days an intranasal (i.n.) challenge with 0.003% active chlorine (in ClO-) or vehicle (distilled water, H2O) was given, followed by assessment of the breathing frequency. One day later, pulmonary function, along with pulmonary inflammation was determined. Lung permeability was assessed by means of total broncho-alveolar lavage (BAL) protein content and plasma surfactant protein (SP)-D levels. In vivo micro-CT imaging revealed enlargement of the lungs and airways early after NA treatment, with a return to normal at day 14. When challenged i.n. with ClO-, NA-pretreated mice immediately responded with a sensory irritant response. Twenty-four hours later, NA/ClO- mice showed airway hyperreactivity (AHR), accompanied by a neutrophilic and eosinophilic inflammation. NA administration followed by ClO- induced airway barrier impairment, as shown by increased BAL protein and plasma SP-D concentrations; histology revealed epithelial denudation. These data prove that NA-induced lung impairment renders the lungs of mice more sensitive to an airway challenge with ClO-, confirming the hypothesis that incomplete barrier repair, followed by irritant exposure results in airway hypersensitivity.
机译：吸入通常存在的刺激物，如氯和氯衍生物，可引起不良呼吸作用，包括刺激诱导的哮喘（IIa）。我们假设由于气道屏障损伤，暴露于次氯酸盐（CLO-）可能导致气道超敏反应。 C57BL / 6小鼠接受腹膜内（I.P.）注射气道损伤剂萘（Na，200mg / kg体重）或载体（矿物油，Mo）。在体内微计算断层扫描（CT）肺之前和在I.P之后的常规时间点获得肺的图像。治疗。在14天的恢复期后，给出了用0.003％活性氯（ClO-）或载体（蒸馏水，H 2 O）攻击，然后评估呼吸频率。一天后，确定肺功能以及肺部炎症。通过全支气管 - 肺泡灌洗（BAL）蛋白质含量和血浆表面活性剂蛋白（SP）-D水平评估肺渗透性。在体内微型CT成像揭示了Na治疗后的肺部和气道的扩大，第14天恢复正常。当挑战I.N.通过Clo-，Na-Preatreated小鼠立即用感觉刺激反应响应。二十四小时后，Na / Clo-小鼠显示气道高反应性（AHR），伴有中性和嗜酸性炎症。 Na AgankeD，随后具有呼吸气道障碍损伤，如增加的BAL蛋白和血浆SP-D浓度所示;组织学揭示了上皮剥落。这些数据证明了Na诱导的肺部损伤使小鼠的肺部对气道挑战更敏感，并确认了阻隔障碍不完全的假设，其次是刺激性的暴露的超敏反应。

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