Enhancement of allergic inflammation by diesel exhaust particles: permissive role of reactive oxygen species

• Published in: Annals of allergy, asthma, & immunology Vol. 83; no. 6 Pt 2; p. 624
• Main Authors: Casillas, A M, Hiura, T, Li, N, Nel, A E
• Format: Journal Article
• Language: English
• Published: United States 01.12.1999
• Subjects: Asthma - etiology; Humans; Reactive Oxygen Species - physiology; Vehicle Emissions - adverse effects
• ISSN: 1081-1206
• DOI: 10.1016/S1081-1206(10)62884-0

Diesel emission particulates (DEP) exert effects on the immune system and act as an adjuvant which enhances allergic inflammation. Animal and human models have delineated the effects of DEP chemicals in enhancing IgE production and promoting T-helper cell-2 (Th2) differentiation. An important primary effect that can explain the DEP-associated humoral and cellular immune responses is the induction of macrophage responses by DEP chemicals. This includes effects on macrophage production of cytokines and chemokines, which may play a role in enhancing allergic inflammation. A potent mechanism in macrophages exposed to DEP chemicals involves the generation of reactive oxygen species (ROS), leading to cellular activation or apoptosis which can be abrogated by antioxidants. These findings may establish a role for antioxidant therapy in diminishing the effects of particulate pollutants in asthma.