title: Role of periostin, FENO, IL-13, lebrikzumab, other IL-13 antagonist and dual IL-4/IL-13 antagonist in asthma.
abstract: BACKGROUND
  Asthma markedly diminishes quality of life due to limited activity, absences from work or school and hospitalizations. Patients with severe asthma which are not controlled despite taking effective therapy are most in need of new treatment approaches. IL-13 was demonstrated as 'central mediator of allergic asthma'.
  
  
  METHODS
  IL-13 has been implicated in the pathogenesis of asthma, idiopathic pulmonary fibrosis and COPD. IL-13 levels in the sputum and bronchial biopsy samples remain elevated in severe asthma despite the use of inhaled and systemic corticosteroids. Thus, IL-13 is a mediator involved in corticosteroid resistance. Periostin enhances profibrotic TGF-β signaling in subepithelial fibrosis associated with asthma. IL-13 induces bronchial epithelial cells to secrete periostin. Periostin may be a biomarker for Th2 induced airway inflammation. Lebrikizumab is a monoclonal antibody against IL-13. Lebrikizumab improved lung function in asthmatics who were symptomatic despite treatment with long acting beta agonist and inhaled corticosteroids and provided benefit in the treatment of severe uncontrolled asthma.
  
  
  CONCLUSIONS
  Lebrikizumab block IL-13 signaling through the IL-13Rα1/IL-4Rα receptor. There was a larger reduction in FENO in the high periostin subgroup than in the low periostin subgroup (34.4 vs 4.3%). Serum CCL17, CCL13 and total IgE levels decreased in the lebrikizumab group.
authors.affiliation: Creighton University, Internal Medicine/Allergy , 601 N 30th Street, Omaha, NE 68131 , USA rtownley@creighton.edu.
authors.forename: Swati
authors.initials: S
authors.lastname: Agrawal
authors.forename: Robert G
authors.initials: RG
authors.lastname: Townley
mesh_terms: D000305:Adrenal Cortex Hormones / Q000737:chemistry; D000818:Animals; D000911:Antibodies, Monoclonal / Q000737:chemistry*; D001249:Asthma / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D001688:Biological Products / Q000627:therapeutic use; D015415:Biomarkers / Q000737:chemistry; D001980:Bronchi / Q000187:drug effects; D015815:Cell Adhesion Molecules / Q000737:chemistry*; D004804:Eosinophils / Q000378:metabolism; D006801:Humans; D006967:Hypersensitivity; D007249:Inflammation; D018793:Interleukin-13 / Q000037:antagonists & inhibitors* / Q000737:chemistry*; D000067596:Interleukin-33; D015847:Interleukin-4 / Q000037:antagonists & inhibitors*; D007378:Interleukins / Q000037:antagonists & inhibitors / Q000737:chemistry; D008168:Lung / Q000187:drug effects; D009569:Nitric Oxide / Q000737:chemistry*; D011788:Quality of Life; D016212:Transforming Growth Factor beta / Q000378:metabolism
chemical_list: D000305:Adrenal Cortex Hormones; D000911:Antibodies, Monoclonal; D001688:Biological Products; D015415:Biomarkers; D015815:Cell Adhesion Molecules; C506536:IL33 protein, human; D018793:Interleukin-13; D000067596:Interleukin-33; D007378:Interleukins; C512835:POSTN protein, human; D016212:Transforming Growth Factor beta; D015847:Interleukin-4; D009569:Nitric Oxide; C561806:lebrikizumab