Department of Medicine, Division of Pulmonary, Allergy, and Critical Care Medicine, Duke University Medical Center, DUMC Box 103004, Durham, NC 27710, USA.
Immunol Res. 2011 Apr;49(1-3):173-91. doi: 10.1007/s12026-010-8180-z.
Ambient ozone is a criteria air pollutant that impacts both human morbidity and mortality. The effect of ozone inhalation includes both toxicity to lung tissue and alteration of the host immunologic response. The innate immune system facilitates immediate recognition of both foreign pathogens and tissue damage. Emerging evidence supports that ozone can modify the host innate immune response and that this response to inhaled ozone is dependent on genes of innate immunity. Improved understanding of the complex interaction between environmental ozone and host innate immunity will provide fundamental insight into the pathogenesis of inflammatory airways disease. We review the current evidence supporting that environmental ozone inhalation: (1) modifies cell types required for intact innate immunity, (2) is partially dependent on genes of innate immunity, (3) primes pulmonary innate immune responses to LPS, and (4) contributes to innate-adaptive immune system cross-talk.
环境臭氧是一种影响人类发病率和死亡率的标准空气污染物。臭氧吸入的影响包括对肺组织的毒性和宿主免疫反应的改变。先天免疫系统有助于对病原体和组织损伤的即时识别。新出现的证据支持臭氧可以改变宿主先天免疫反应，并且这种对吸入臭氧的反应依赖于先天免疫基因。更好地了解环境臭氧和宿主先天免疫之间的复杂相互作用，将为炎症性气道疾病的发病机制提供基本的认识。我们回顾了支持以下观点的现有证据：（1）改变了完整先天免疫所需的细胞类型；（2）部分依赖于先天免疫基因；（3）使肺部先天免疫对 LPS 产生反应；（4）有助于先天-适应性免疫系统的交叉对话。
