Martin L D, Krunkosky T M, Voynow J A, Adler K B
Department of Anatomy, Physiological Sciences, and Radiology, College of Veterinary Medicine, North Carolina State University, Raleigh 27606, USA.
Environ Health Perspect. 1998 Oct;106 Suppl 5(Suppl 5):1197-203. doi: 10.1289/ehp.98106s51197.
The body first encounters deleterious inhaled substances, such as allergens, industrial particles, pollutants, and infectious agents, at the airway epithelium. When this occurs, the epithelium and its resident inflammatory cells respond defensively by increasing production of cytokines, mucus, and reactive oxygen and nitrogen species (ROS/RNS). As inflammation in the airway increases, additional infiltrating cells increase the level of these products. Recent interest has focused on ROS/RNS as potential modulators of the expression of inflammation-associated genes important to the pathogenesis of various respiratory diseases. ROS/RNS appear to play a variety of roles that lead to changes in expression of genes such as interleukin-6 and intercellular adhesion molecule 1. By controlling this regulation, the reactive species can serve as exogenous stimuli, as intercellular signaling molecules, and as modulators of the redox state in epithelial cells. Unraveling the molecular mechanisms affected by ROS/RNS acting in these capacities should aid in the understanding of how stimulated defense mechanisms within the airway can lead to disease.
人体首次接触有害吸入物质，如过敏原、工业颗粒、污染物和传染原，是在气道上皮。当这种情况发生时，上皮及其驻留的炎症细胞会通过增加细胞因子、黏液以及活性氧和氮物质（ROS/RNS）的产生来做出防御反应。随着气道炎症加剧，更多浸润细胞会增加这些产物的水平。最近的研究兴趣集中在ROS/RNS作为对各种呼吸系统疾病发病机制至关重要的炎症相关基因表达的潜在调节因子。ROS/RNS似乎发挥着多种作用，导致白细胞介素-6和细胞间黏附分子1等基因表达发生变化。通过控制这种调节，活性物质可作为外源性刺激物、细胞间信号分子以及上皮细胞氧化还原状态的调节剂。阐明受ROS/RNS以这些能力作用影响的分子机制，应有助于理解气道内受刺激的防御机制如何导致疾病。
