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臭氧对特应性与非特应性豚鼠的气道反应性有不同的调节作用。

Ozone differentially modulates airway responsiveness in atopic versus nonatopic guinea pigs.

作者信息

Schlesinger Richard B, Cohen Mitchell D, Gordon Terry, Nadziejko Christine, Zelikoff Judith T, Sisco Maureen, Regal Jean F, Ménache Margaret G

机构信息

Department of Environmental Medicine, New York University School of Medicine, 57 Old Forge Road, Tuxedo, NY 10987, USA.

出版信息

Inhal Toxicol. 2002 May;14(5):431-57. doi: 10.1080/089583701753678562.

DOI:10.1080/089583701753678562
PMID:12028802
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2978653/
Abstract

While acute exposures to ozone (O(3)) can alter airway responsiveness, effects from long-term exposures at low concentrations are less clear. This study assessed whether such exposures could induce nonspecific hyperresponsiveness in nonatopic (nonsensitized) guinea pigs and/or could exacerbate the pre-existing hyperresponsive state in atopic (sensitized) animals, and whether gender was a factor modulating any effect of O(3). Responsiveness was measured during and following exposures to 0.1 and 0.3 ppm O(3) for 4 h/day, 4 days/wk for 24 wk in male and female nonsensitized animals, those sensitized to allergen (ovalbumin) prior to initiation of O(3) exposures, and those sensitized concurrently with exposures. Ozone did not produce hyperresponsiveness in nonsensitized animals, but did exacerbate hyperresponsiveness to both specific and nonspecific bronchoprovocation challenges in sensitized animals, an effect that persisted through at least 4 wk after exposures ended. Gender was not a factor modulating response to O(3). Induced effects on responsiveness were not associated with numbers of eosinophils in the lungs nor with any chronic pulmonary inflammatory response, but were correlated with antigen-specific antibodies in blood. This study supports a role for chronic O(3) exposure in the exacerbation of airways dysfunction in a certain segment of the general population, namely, those demonstrating atopy.

摘要

虽然急性暴露于臭氧(O₃)会改变气道反应性,但低浓度长期暴露的影响尚不清楚。本研究评估了这种暴露是否会在非特应性(未致敏)豚鼠中诱导非特异性高反应性和/或是否会加重特应性(致敏)动物中已有的高反应状态,以及性别是否是调节O₃任何作用的一个因素。在雄性和雌性未致敏动物、在开始O₃暴露之前对过敏原(卵清蛋白)致敏的动物以及在暴露同时致敏的动物中,测量了在每天4小时、每周4天、持续24周暴露于0.1和0.3 ppm O₃期间及之后的反应性。臭氧在未致敏动物中未产生高反应性,但确实加重了致敏动物对特异性和非特异性支气管激发试验的高反应性,这种效应在暴露结束后至少持续4周。性别不是调节对O₃反应的一个因素。对反应性的诱导作用与肺中嗜酸性粒细胞数量无关,也与任何慢性肺部炎症反应无关,但与血液中的抗原特异性抗体相关。本研究支持慢性O₃暴露在加重一般人群中某一特定部分(即表现出特应性的人群)的气道功能障碍中所起的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa2d/2978653/1d4377e43de2/nihms242941f7.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa2d/2978653/1f3ecf0f0813/nihms242941f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa2d/2978653/54dd923c122e/nihms242941f2.jpg
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本文引用的文献

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