Suppr超能文献

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.

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。

相似文献

1
Postnatal episodic ozone results in persistent attenuation of pulmonary and peripheral blood responses to LPS challenge.
Am J Physiol Lung Cell Mol Physiol. 2011 Mar;300(3):L462-71. doi: 10.1152/ajplung.00254.2010. Epub 2010 Dec 3.
2
Early life ozone exposure results in dysregulated innate immune function and altered microRNA expression in airway epithelium.
PLoS One. 2014 Mar 4;9(3):e90401. doi: 10.1371/journal.pone.0090401. eCollection 2014.
3
Ozone and allergen exposure during postnatal development alters the frequency and airway distribution of CD25+ cells in infant rhesus monkeys.
Toxicol Appl Pharmacol. 2009 Apr 1;236(1):39-48. doi: 10.1016/j.taap.2008.12.031. Epub 2009 Feb 7.
4
Early life allergen and air pollutant exposures alter longitudinal blood immune profiles in infant rhesus monkeys.
Toxicol Appl Pharmacol. 2017 Aug 1;328:60-69. doi: 10.1016/j.taap.2017.05.006. Epub 2017 May 18.
5
Ambient ozone primes pulmonary innate immunity in mice.
J Immunol. 2007 Oct 1;179(7):4367-75. doi: 10.4049/jimmunol.179.7.4367.
6
Protective Role of Eosinophils and TNFa after Ozone Inhalation.
Res Rep Health Eff Inst. 2017 Mar;2017(191):1-41.
7
Ozone-induced airway epithelial cell death, the neurokinin-1 receptor pathway, and the postnatal developing lung.
Am J Physiol Lung Cell Mol Physiol. 2014 Sep 15;307(6):L471-81. doi: 10.1152/ajplung.00324.2013. Epub 2014 Jul 25.
10
Postnatal lung development: immediate-early gene responses post ozone and LPS exposure.
Inhal Toxicol. 2006 Oct;18(11):875-83. doi: 10.1080/08958370600822466.

引用本文的文献

1
Early Life Wildfire Smoke Exposure Is Associated with Immune Dysregulation and Lung Function Decrements in Adolescence.
Am J Respir Cell Mol Biol. 2017 May;56(5):657-666. doi: 10.1165/rcmb.2016-0380OC.
2
Cyclic Ozone Exposure Induces Gender-Dependent Neuropathology and Memory Decline in an Animal Model of Alzheimer's Disease.
Toxicol Sci. 2015 Sep;147(1):222-34. doi: 10.1093/toxsci/kfv124. Epub 2015 Jun 26.
3
Ozone inhalation modifies the rat liver proteome.
Redox Biol. 2014;2:52-60. doi: 10.1016/j.redox.2013.11.006. Epub 2013 Nov 28.
4
Why primate models matter.
Am J Primatol. 2014 Sep;76(9):801-27. doi: 10.1002/ajp.22281. Epub 2014 Apr 10.
5
Early life ozone exposure results in dysregulated innate immune function and altered microRNA expression in airway epithelium.
PLoS One. 2014 Mar 4;9(3):e90401. doi: 10.1371/journal.pone.0090401. eCollection 2014.
6
Transcriptome profiling of the newborn mouse lung response to acute ozone exposure.
Toxicol Sci. 2014 Mar;138(1):175-90. doi: 10.1093/toxsci/kft276. Epub 2013 Dec 12.
7
Innate immune response to LPS in airway epithelium is dependent on chronological age and antecedent exposures.
Am J Respir Cell Mol Biol. 2013 Nov;49(5):710-20. doi: 10.1165/rcmb.2012-0321OC.

本文引用的文献

1
Early life activation of toll-like receptor 4 reprograms neural anti-inflammatory pathways.
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.
PLoS One. 2010 Apr 28;5(4):e10407. doi: 10.1371/journal.pone.0010407.
3
MicroRNAs distinguish translational from transcriptional silencing during endotoxin tolerance.
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.
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.
Environ Res. 2010 Apr;110(3):294-301. doi: 10.1016/j.envres.2010.01.001. Epub 2010 Feb 1.
9
Maternal exposure to particulate matter increases postnatal ozone-induced airway hyperreactivity in juvenile mice.
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.
Am J Respir Cell Mol Biol. 2010 Apr;42(4):424-31. doi: 10.1165/rcmb.2008-0408OC. Epub 2009 Jun 5.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验