Nikasinovic L, Momas I, Just J
Laboratoire d'Hygiène et de Santé Publique, Faculté des Sciences Pharmaceutiques et Biologiques, Université René Descartes, Paris, France.
J Toxicol Environ Health B Crit Rev. 2004 Mar-Apr;7(2):81-104. doi: 10.1080/10937400490241952.
The aim of the present review is to summarize biological events in nasal epithelium after short-term exposure to diesel exhaust particles (DEP). Therefore human, animal, and in vitro studies carried out since 1987 are reviewed. Short-term exposure results included qualitative alterations characterized by immediate nasal hyperresponsiveness, antioxidant responses, marked epithelial inflammation, and a specific humoral response. In addition, studies on combined DEP/allergen challenge reported that, besides their intrinsic deleterious properties, DEP produced adjuvant-like effects on the immediate and late-phase response to allergen challenge, since they are able to mimic effects occurring after allergen challenge. DEP act deeply in nasal epithelium by (1) directing cytokine gene expression toward a Th2 profile, (2) enhancing local antigen-specific immunoglobulin E (IgE) production, and (3) driving in vivo isotype switch to IgE. Furthermore, DEP can induce in allergic subjects sensitization to a neoallergen, sensitization that did not occur with exposure to the neoantigen alone. Particulate pollutants such as DEP, encountered in urban areas, are therefore thought to be contributing causal factors to the exaggerated sensitization to allergens in subjects with appropriate genetic predisposition, sensitization that they might not otherwise have experienced. These findings add weight to the hypothesis that DEP are involved in the increased prevalence of airway allergic diseases.
本综述的目的是总结短期暴露于柴油废气颗粒(DEP)后鼻上皮中的生物学事件。因此,对自1987年以来进行的人体、动物和体外研究进行了综述。短期暴露结果包括定性改变,其特征为立即出现鼻高反应性、抗氧化反应、明显的上皮炎症和特异性体液反应。此外,关于DEP/过敏原联合激发的研究报告称,除了其固有的有害特性外,DEP对过敏原激发的即刻和迟发反应产生佐剂样作用,因为它们能够模拟过敏原激发后出现的效应。DEP通过以下方式在鼻上皮中产生深刻作用:(1)将细胞因子基因表达导向Th2谱;(2)增强局部抗原特异性免疫球蛋白E(IgE)的产生;(3)驱动体内向IgE的同种型转换。此外,DEP可在过敏受试者中诱导对新过敏原的致敏,而单独暴露于新抗原时不会发生这种致敏。因此,城市地区遇到的诸如DEP之类的颗粒污染物被认为是导致具有适当遗传易感性的受试者对过敏原过度致敏的因果因素,否则他们可能不会经历这种致敏。这些发现进一步支持了DEP与气道过敏性疾病患病率增加有关的假说。