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出生后早期接触过敏原和臭氧会导致肺上皮神经支配过度。

Early postnatal exposure to allergen and ozone leads to hyperinnervation of the pulmonary epithelium.

作者信息

Kajekar Radhika, Pieczarka Emily M, Smiley-Jewell Suzette M, Schelegle Edward S, Fanucchi Michelle V, Plopper Charles G

机构信息

Center for Comparative Respiratory Biology and Medicine, School of Veterinary Medicine, University of California, Davis, CA 95616, USA.

出版信息

Respir Physiol Neurobiol. 2007 Jan 15;155(1):55-63. doi: 10.1016/j.resp.2006.03.002. Epub 2006 Apr 17.

DOI:10.1016/j.resp.2006.03.002
PMID:16616710
Abstract

Airway injury in infant monkeys exposed to ozone and/or house dust mite allergen (HDMA) is associated with a loss of epithelial innervation. In this study, we evaluated for persistence/recovery of the altered epithelial innervation. Thirty-day-old rhesus monkeys were exposed to repeated episodes of HDMA and/or ozone from 1 to 6 months of age and subsequently allowed to recover for 6 months in the absence of further ozone exposure and/or minimal HDMA challenge (sufficient to maintain allergen sensitization). At 1 year of age, nerve density in intrapulmonary airways was immunohistochemically evaluated using antibodies directed against protein gene product 9.5. Hyperinnervation and irregular epithelial nerve distribution was observed in both HDMA- and ozone-exposed groups; most prominent alterations were observed in animals exposed to HDMA plus ozone. Therefore, while adaptive mechanisms exist that re-establish epithelial innervation following cessation or diminution of exposure to HDMA and/or ozone, the recovery is associated with persistent proliferative mechanisms that result in hyperinnervation of the airways.

摘要

暴露于臭氧和/或屋尘螨变应原(HDMA)的幼猴气道损伤与上皮神经支配丧失有关。在本研究中,我们评估了改变的上皮神经支配的持续存在/恢复情况。30日龄恒河猴在1至6月龄时反复暴露于HDMA和/或臭氧,随后在无进一步臭氧暴露和/或最小HDMA激发(足以维持变应原致敏)的情况下恢复6个月。1岁时,使用针对蛋白基因产物9.5的抗体通过免疫组织化学评估肺内气道的神经密度。在HDMA和臭氧暴露组中均观察到神经支配过度和上皮神经分布不规则;在暴露于HDMA加臭氧的动物中观察到最明显的改变。因此,虽然存在适应性机制,在停止或减少HDMA和/或臭氧暴露后重新建立上皮神经支配,但恢复与导致气道神经支配过度的持续增殖机制有关。

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