The role of reactive oxygen and nitrogen species in airway epithelial gene expression.

Published

Journal Article (Review)

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.

Full Text

Cited Authors

  • Martin, LD; Krunkosky, TM; Voynow, JA; Adler, KB

Published Date

  • October 1998

Published In

Volume / Issue

  • 106 Suppl 5 /

Start / End Page

  • 1197 - 1203

PubMed ID

  • 9788898

Pubmed Central ID

  • 9788898

Electronic International Standard Serial Number (EISSN)

  • 1552-9924

International Standard Serial Number (ISSN)

  • 0091-6765

Digital Object Identifier (DOI)

  • 10.1289/ehp.98106s51197

Language

  • eng