title: Airway inflammation and eotaxin in exhaled breath condensate of patients with severe persistent allergic asthma during omalizumab therapy.
abstract: OBJECTIVE
  The central role of IgE in allergic inflammation in asthma has provided a rationale for the development of omalizumab, the humanized monoclonal anti-IgE antibody. The aim of the study was to determine the effect of omalizumab treatment on changes in airway inflammatory process and eotaxin in exhaled breath condensate in patients with persistent severe allergic asthma.
  
  
  METHODS
  The study was performed on a group of 19 patients with severe persistent allergic asthma treated with conventional therapy (according to GINA 2006) and with or without omalizumab (9 vs 10 patients). Eotaxin in exhaled breath condensate, exhaled nitric oxide, blood eosinophil count and serum ECP were measured before and after 16 weeks of therapy.
  
  
  RESULTS
  In the group treated with omalizumab, a statistically significant decrease in the concentrations of eotaxin in EBC, FENO, serum ECP, and blood eosinophil count after 16 weeks of treatment was observed. Statistically significant correlations were revealed between the decrease in eotaxin and the decrease in FENO, serum ECP and blood eosinophil count after omalizumab therapy.
  
  
  CONCLUSIONS
  Downregulation of eotaxin expression in the airways through limitation of eosinophilic inflammation could be essential in the beneficial effect of anti-IgE therapy with omalizumab in asthma patients.
authors.affiliation: Department of Allergology and Internal Medicine, Medical University of Bialystok, Poland. z.zietkowski@wp.pl
authors.forename: Z
authors.initials: Z
authors.lastname: Zietkowski
authors.forename: R
authors.initials: R
authors.lastname: Skiepko
authors.forename: M M
authors.initials: MM
authors.lastname: Tomasiak-Lozowska
authors.forename: A
authors.initials: A
authors.lastname: Bodzenta-Lukaszyk
mesh_terms: D000328:Adult; D018926:Anti-Allergic Agents / Q000494:pharmacology; D000888:Antibodies, Anti-Idiotypic / Q000494:pharmacology*; D000911:Antibodies, Monoclonal / Q000737:chemistry; D061067:Antibodies, Monoclonal, Humanized / Q000494:pharmacology*; D054413:Chemokine CCL11 / Q000378:metabolism*; D004804:Eosinophils / Q000378:metabolism; D045853:Exhalation; D005260:Female; D006801:Humans; D006967:Hypersensitivity / Q000378:metabolism; D007073:Immunoglobulin E / Q000737:chemistry / Q000276:immunology*; D007249:Inflammation / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000378:metabolism; D000069444:Omalizumab; D013997:Time Factors
chemical_list: D018926:Anti-Allergic Agents; D000888:Antibodies, Anti-Idiotypic; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; C515456:CCL11 protein, human; D054413:Chemokine CCL11; D000069444:Omalizumab; D009569:Nitric Oxide; D007073:Immunoglobulin E