title: Omalizumab attenuates airway inflammation and interleukin-5 production by mononuclear cells in patients with severe allergic asthma.
abstract: BACKGROUND
  Omalizumab, an anti-immunoglobulin E monoclonal antibody, has shown an inhibitory effect on airway inflammation, which may be associated with clinical improvement of severe asthma. This study evaluated changes in airway inflammation and cytokine release by the peripheral blood mononuclear cells (PBMCs) of Japanese patients with severe asthma after administration of omalizumab.
  
  
  METHODS
  Sixteen Japanese patients with severe asthma who were allergic to house-dust mites were enrolled in this study. Eight received omalizumab every 2 or 4 weeks for 16 weeks, and 8 control subjects were treated with conventional drug treatment. Changes in clinical scores for sputum eosinophils and levels of fraction of exhaled nitric oxide (FeNO) were measured at the time of enrollment and at week 16. Cytokines from PBMCs stimulated by house-dust mite (Dermatophagoides farinae) or ionomycin/phorbol myristate acetate (PMA) were measured at baseline and at week 16.
  
  
  RESULTS
  In the omalizumab-treated group, decreases in sputum eosinophils and FeNO were observed following treatment. Furthermore, the ex vivo production of interleukin (IL)-5 by PBMCs in response to both mite allergen and ionomycin/PMA decreased significantly. In contrast, interferon (IFN)-γ production was unchanged. There were no changes in any of the parameters observed in the control group.
  
  
  CONCLUSIONS
  Omalizumab exerts inhibitory effects on airway inflammation in Japanese patients with severe allergic asthma. This treatment attenuates production of IL-5 by PBMCs stimulated with both a specific allergen and a nonspecific activator. Reduction of the Th2 inflammatory cascade likely contributes to clinical benefits; however, further studies are required to clarify these results due to the small sample size in this study.
authors.affiliation: Allergy Center, Saitama Medical University, Saitama, Japan.
authors.forename: Yotaro
authors.initials: Y
authors.lastname: Takaku
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Soma
authors.forename: Fuyumi
authors.initials: F
authors.lastname: Nishihara
authors.forename: Kazuyuki
authors.initials: K
authors.lastname: Nakagome
authors.forename: Takehito
authors.initials: T
authors.lastname: Kobayashi
authors.forename: Koichi
authors.initials: K
authors.lastname: Hagiwara
authors.forename: Minoru
authors.initials: M
authors.lastname: Kanazawa
authors.forename: Makoto
authors.initials: M
authors.lastname: Nagata
mesh_terms: D000328:Adult; D018927:Anti-Asthmatic Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D000888:Antibodies, Anti-Idiotypic / Q000008:administration & dosage / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized / Q000008:administration & dosage / Q000627:therapeutic use*; D001249:Asthma / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism*; D016207:Cytokines / Q000096:biosynthesis; D005260:Female; D006801:Humans; D015848:Interleukin-5 / Q000096:biosynthesis*; D007963:Leukocytes, Mononuclear / Q000276:immunology / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D000069444:Omalizumab; D011446:Prospective Studies; D016896:Treatment Outcome
chemical_list: D018927:Anti-Asthmatic Agents; D000888:Antibodies, Anti-Idiotypic; D061067:Antibodies, Monoclonal, Humanized; D016207:Cytokines; D015848:Interleukin-5; D000069444:Omalizumab