title: Importance of oxidative stress in the pathogenesis and treatment of asthma.
abstract: OBJECTIVE
  The purpose of the current review is to summarize recent evidence demonstrating the important role of oxidative stress in asthma pathogenesis. The therapeutic implications of these findings will be presented.
  
  
  RESULTS
  Mechanistically, the effect of oxidative stress on dendritic cells has been demonstrated to have a potent effect on Th1/Th2 skewing of the immune response. Investigations of gene-environment interactions have identified genetic polymorphisms associated with individual susceptibility to pollutant-induced respiratory oxidative stress. The effects of current asthma therapy on oxidative stress are currently unclear, but previous trials using conventional antioxidant therapy in asthma have been largely ineffective. Recent investigations have identified two promising broad-based therapeutic approaches: Nrf2 pathway activation and the use of thiol precursors. Preliminary data suggest that fullerene nanomaterials and dietary interventions may also have potential benefits in asthma.
  
  
  CONCLUSIONS
  Our current understanding of the role of oxidative stress in asthma suggests that antioxidant therapy may be important in optimizing asthma treatment and prevention. The future success of antioxidant asthma therapy will require strategies with broad effects on airway redox equilibrium and the selection of appropriate target populations.
authors.affiliation: Section of Clinical Immunology and Allergy, Division of Pulmonary and Critical Care Medicine, UCLA David Geffen School of Medicine, Los Angeles, California 90095, USA. mriedl@mednet.ucla.edu
authors.forename: Marc A
authors.initials: MA
authors.lastname: Riedl
authors.forename: Andre E
authors.initials: AE
authors.lastname: Nel
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism / Q000627:therapeutic use; D001249:Asthma / Q000235:genetics / Q000276:immunology* / Q000503:physiopathology* / Q000628:therapy*; D002454:Cell Differentiation / Q000276:immunology; D004249:DNA Damage; D003713:Dendritic Cells / Q000276:immunology* / Q000473:pathology; D005247:Feeding Behavior; D037741:Fullerenes / Q000627:therapeutic use; D020022:Genetic Predisposition to Disease; D006801:Humans; D051379:Mice; D018345:Mice, Knockout; D018448:Models, Immunological; D051267:NF-E2-Related Factor 2 / Q000235:genetics / Q000276:immunology; D018384:Oxidative Stress / Q000187:drug effects / Q000235:genetics / Q000276:immunology; D017382:Reactive Oxygen Species / Q000037:antagonists & inhibitors / Q000378:metabolism; D013438:Sulfhydryl Compounds / Q000627:therapeutic use; D015533:Transcriptional Activation
chemical_list: D000975:Antioxidants; D037741:Fullerenes; D051267:NF-E2-Related Factor 2; C495635:NFE2L2 protein, human; D017382:Reactive Oxygen Species; D013438:Sulfhydryl Compounds