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Am J Physiol Lung Cell Mol Physiol. 2011 Mar;300(3):L462-71. doi: 10.1152/ajplung.00254.2010. Epub 2010 Dec 3.
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本文引用的文献

1
Early life activation of toll-like receptor 4 reprograms neural anti-inflammatory pathways.早期生命中 Toll 样受体 4 的激活会重新编程神经抗炎途径。
J Neurosci. 2010 Jun 9;30(23):7975-83. doi: 10.1523/JNEUROSCI.6078-09.2010.
2
Acquisition of adult-like TLR4 and TLR9 responses during the first year of life.在生命的第一年获得成人样 TLR4 和 TLR9 反应。
PLoS One. 2010 Apr 28;5(4):e10407. doi: 10.1371/journal.pone.0010407.
3
MicroRNAs distinguish translational from transcriptional silencing during endotoxin tolerance.微小 RNA 在内毒素耐受期间区分翻译和转录沉默。
J Biol Chem. 2010 Jul 2;285(27):20940-51. doi: 10.1074/jbc.M110.115063. Epub 2010 Apr 30.
4
Ozone activates pulmonary dendritic cells and promotes allergic sensitization through a Toll-like receptor 4-dependent mechanism.臭氧通过 Toll 样受体 4 依赖机制激活肺部树突状细胞并促进过敏敏化。
J Allergy Clin Immunol. 2010 May;125(5):1167-70. doi: 10.1016/j.jaci.2010.03.001. Epub 2010 Apr 15.
5
The association between childhood asthma prevalence and monitored air pollutants in metropolitan areas, United States, 2001-2004.美国大都市地区 2001-2004 年儿童哮喘患病率与监测空气污染物的关系。
Environ Res. 2010 Apr;110(3):294-301. doi: 10.1016/j.envres.2010.01.001. Epub 2010 Feb 1.
6
The influence of age and sex on the cell counts of peripheral blood leukocyte subpopulations in Chinese rhesus macaques.年龄和性别对中国恒河猴外周血白细胞亚群细胞计数的影响。
Cell Mol Immunol. 2009 Dec;6(6):433-40. doi: 10.1038/cmi.2009.55.
7
Cellular and molecular characterization of ozone-induced pulmonary inflammation in the Cynomolgus monkey.臭氧诱导食蟹猴肺部炎症的细胞和分子特征。
Inflammation. 2010 Jun;33(3):144-56. doi: 10.1007/s10753-009-9168-5.
8
Parental characteristics, somatic fetal growth, and season of birth influence innate and adaptive cord blood cytokine responses.父母特征、胎儿躯体生长及出生季节影响脐带血固有免疫和适应性免疫细胞因子反应。
J Allergy Clin Immunol. 2009 Nov;124(5):1078-87. doi: 10.1016/j.jaci.2009.08.021.
9
Maternal exposure to particulate matter increases postnatal ozone-induced airway hyperreactivity in juvenile mice.母体暴露于颗粒物会增加幼鼠出生后臭氧诱导的气道高反应性。
Am J Respir Crit Care Med. 2009 Dec 15;180(12):1218-26. doi: 10.1164/rccm.200901-0116OC. Epub 2009 Sep 17.
10
TLR-4-mediated innate immunity is reduced in cystic fibrosis airway cells.TLR-4 介导的固有免疫在囊性纤维化气道细胞中降低。
Am J Respir Cell Mol Biol. 2010 Apr;42(4):424-31. doi: 10.1165/rcmb.2008-0408OC. Epub 2009 Jun 5.

产后间歇性臭氧暴露导致对 LPS 挑战的肺和外周血反应持续减弱。

Postnatal episodic ozone results in persistent attenuation of pulmonary and peripheral blood responses to LPS challenge.

机构信息

California National Primate Research Center, Univ. of California, Davis, 95616, USA.

出版信息

Am J Physiol Lung Cell Mol Physiol. 2011 Mar;300(3):L462-71. doi: 10.1152/ajplung.00254.2010. Epub 2010 Dec 3.

DOI:10.1152/ajplung.00254.2010
PMID:21131396
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3064293/
Abstract

Early life is a dynamic period of growth for the lung and immune system. We hypothesized that ambient ozone exposure during postnatal development can affect the innate immune response to other environmental challenges in a persistent fashion. To test this hypothesis, we exposed infant rhesus macaque monkeys to a regimen of 11 ozone cycles between 30 days and 6 mo of age; each cycle consisted of ozone for 5 days (0.5 parts per million at 8 h/day) followed by 9 days of filtered air. Animals were subsequently housed in filtered air conditions and challenged with a single dose of inhaled LPS at 1 yr of age. After completion of the ozone exposure regimen at 6 mo of age, total peripheral blood leukocyte and polymorphonuclear leukocyte (PMN) numbers were reduced, whereas eosinophil counts increased. In lavage, total cell numbers at 6 mo were not affected by ozone, however, there was a significant reduction in lymphocytes and increased eosinophils. Following an additional 6 mo of filtered air housing, only monocytes were increased in blood and lavage in previously exposed animals. In response to LPS challenge, animals with a prior history of ozone showed an attenuated peripheral blood and lavage PMN response compared with controls. In vitro stimulation of peripheral blood mononuclear cells with LPS resulted in reduced secretion of IL-6 and IL-8 protein in association with prior ozone exposure. Collectively, our findings suggest that ozone exposure during infancy can result in a persistent effect on both pulmonary and systemic innate immune responses later in life.

摘要

生命早期是肺部和免疫系统生长的活跃时期。我们假设,在出生后发育过程中暴露于环境臭氧会以持续的方式影响对其他环境挑战的固有免疫反应。为了验证这一假设,我们在 30 天至 6 月龄期间使幼年恒河猴暴露于 11 个臭氧循环的方案中;每个循环包括 5 天的臭氧暴露(8 小时/天,0.5 个百万分率),随后是 9 天的过滤空气。动物随后被安置在过滤空气条件下,并在 1 岁时接受单次吸入 LPS 挑战。在 6 月龄完成臭氧暴露方案后,外周血白细胞和多形核白细胞(PMN)数量减少,而嗜酸性粒细胞计数增加。在灌洗中,臭氧对 6 月龄的总细胞数没有影响,但是淋巴细胞减少,嗜酸性粒细胞增加。在经过另外 6 个月的过滤空气饲养后,仅在先前暴露的动物中,血液和灌洗中的单核细胞增加。在 LPS 挑战后,与对照组相比,有先前臭氧暴露史的动物表现出外周血和灌洗 PMN 反应减弱。体外用 LPS 刺激外周血单核细胞导致与先前臭氧暴露相关的 IL-6 和 IL-8 蛋白分泌减少。总的来说,我们的发现表明,婴儿期暴露于臭氧会导致生命后期肺部和全身固有免疫反应产生持久影响。