title: Therapeutic implications of 'neutrophilic asthma'.
abstract: OBJECTIVE
  This review examines the association between airway neutrophilia and severe asthma, potential mechanisms, and the effect on asthma control of therapies directed at reducing airway neutrophil numbers or activity.
  
  
  RESULTS
  The majority of studies that observe an association between airway neutrophilia and severe asthma are cross-sectional in nature, and the intensity of neutrophilia is low and may be a reflection of the age of the patients, effect of tobacco smoke exposure, or the high doses of corticosteroids used to treat their asthma. There may be a small proportion of patients who may have abnormal innate immune responses that may lead to airway neutrophilia. However, these neutrophils may not be any more activated than in patients with milder asthma. Novel strategies using small molecule antagonists against the interleukin-8 receptor, CXCR2, are able to reduce airway neutrophilia, and their clinical efficacies are being investigated.
  
  
  CONCLUSIONS
  Although cross-sectional studies suggest that airway neutrophilia may be observed in some patients with severe asthma, it is not clearly established if this is a consequence of treatment with corticosteroids or if it contributes directly to asthma pathobiology and severity. New therapies such as anti-CXCR2 provide an opportunity to investigate the contribution of neutrophils to asthma severity.
authors.affiliation: Firestone Institute for Respiratory Health, St. Joseph's Healthcare and Department of Medicine, McMaster University, Hamilton, Ontario, Canada.
authors.forename: Parameswaran
authors.initials: P
authors.lastname: Nair
authors.forename: Afia
authors.initials: A
authors.lastname: Aziz-Ur-Rehman
authors.forename: Katherine
authors.initials: K
authors.lastname: Radford
mesh_terms: D000367:Age Factors; D018927:Anti-Asthmatic Agents / Q000627:therapeutic use*; D001249:Asthma / Q000188:drug therapy / Q000276:immunology* / Q000503:physiopathology; D003430:Cross-Sectional Studies; D018450:Disease Progression; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation / Q000188:drug therapy / Q000276:immunology* / Q000503:physiopathology; D018836:Inflammation Mediators / Q000276:immunology* / Q000378:metabolism; D009504:Neutrophils / Q000378:metabolism*; D023063:Receptors, Interleukin-8B / Q000187:drug effects*; D018570:Risk Assessment; D012720:Severity of Illness Index; D012907:Smoking / Q000009:adverse effects; D013183:Sputum / Q000276:immunology
chemical_list: D018927:Anti-Asthmatic Agents; D018836:Inflammation Mediators; D023063:Receptors, Interleukin-8B