title: Ozone therapy effects on biomarkers and lung function in asthma.
abstract: BACKGROUND
  The relationship and behavior of serum immunoglobulin E (IgE) level, peripheral blood mononuclear cell (PBMC) human leukocyte antigen DR (HLA-DR) expression and erythrocyte glutathione antioxidant pathway in asthma patients treated with systemic ozone therapy have not been studied before.
  
  
  METHODS
  Asthma patients were treated about 1 year with three cycles (5 or 6 months each) with three different ozone therapy protocols. Ozone major autohemotherapy (MAHT) was applied at doses of 4 and 8 mg, 15 sessions each cycle; and ozone rectal insufflations (RI) at a dose of 10 mg, 20 sessions each cycle. Serum IgE, HLA-DR expression in PBMC and biomarkers for antioxidant pathway were measured before and at the end of each cycle. Lung function and symptoms test were recorded at the beginning and after the third cycle.
  
  
  RESULTS
  IgE and HLA-DR decreased with the three types of treatments, while increments in reduced glutathione, glutathione peroxidase, glutation reductase and glutathione S-transferase were achieved with all treatments. Lung function and symptoms test were markedly improved. However, in all parameters the best response was obtained in the order: MAHT at 8 mg better than MAHT at 4 mg better than RI at 10 mg. Before ozone treatment, glutathione antioxidant parameters were under the normal reference values, suggesting the occurrence of oxidative stress associated with atopic asthma.
  
  
  CONCLUSIONS
  This study demonstrates the effectiveness of ozone therapy in reducing IgE and inflammatory mediators along with the induction of antioxidant elements. The study raises the role of systemic ozone therapy in atopic asthma by means of its immunomodulatory and oxidative stress regulation properties.
authors.affiliation: Departmento de Biomedicina, Centro de Investigaciones del Ozono del Centro Nacional de Investigaciones Científicas, Ciudad de la Habana, Cuba. frank.hernandez@cnic.edu.cu
authors.forename: Frank A
authors.initials: FA
authors.lastname: Hernández Rosales
authors.forename: José L
authors.initials: JL
authors.lastname: Calunga Fernández
authors.forename: José
authors.initials: J
authors.lastname: Turrent Figueras
authors.forename: Silvia
authors.initials: S
authors.lastname: Menéndez Cepero
authors.forename: Adonis
authors.initials: A
authors.lastname: Montenegro Perdomo
mesh_terms: D000293:Adolescent; D000328:Adult; D000975:Antioxidants / Q000378:metabolism; D001249:Asthma / Q000276:immunology / Q000628:therapy*; D015415:Biomarkers; D016535:Bronchial Hyperreactivity; D005260:Female; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D006684:HLA-DR Antigens / Q000097:blood / Q000276:immunology; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood / Q000276:immunology; D008168:Lung / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D010083:Oxidants, Photochemical / Q000627:therapeutic use*; D010126:Ozone / Q000627:therapeutic use*
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D006684:HLA-DR Antigens; D010083:Oxidants, Photochemical; D007073:Immunoglobulin E; D010126:Ozone; D005979:Glutathione Peroxidase; D005980:Glutathione Reductase; D005982:Glutathione Transferase; D005978:Glutathione