title: Non-eosinophilic asthma: importance and possible mechanisms.
abstract: There is increasing evidence that inflammatory mechanisms other than eosinophilic inflammation may be involved in producing the final common pathway of enhanced bronchial reactivity and reversible airflow obstruction that characterises asthma. A review of the literature has shown that, at most, only 50% of asthma cases are attributable to eosinophilic airway inflammation. It is hypothesised that a major proportion of asthma is based on neutrophilic airway inflammation, possibly triggered by environmental exposure to bacterial endotoxin, particulate air pollution, and ozone, as well as viral infections. If there are indeed two (or more) subtypes of asthma, and if non-eosinophilic (neutrophil mediated) asthma is relatively common, this would have major consequences for the treatment and prevention of asthma since most treatment and prevention strategies are now almost entirely focused on allergic/eosinophilic asthma and allergen avoidance measures, respectively. It is therefore important to study the aetiology of asthma further, including the underlying inflammatory profiles.
authors.affiliation: Institute for Risk Assessment Sciences (IRAS), Division of Environmental and Occupational Health, Utrecht University, The Netherlands. j.douwes@iras.uu.nl
authors.forename: J
authors.initials: J
authors.lastname: Douwes
authors.forename: P
authors.initials: P
authors.lastname: Gibson
authors.forename: J
authors.initials: J
authors.lastname: Pekkanen
authors.forename: N
authors.initials: N
authors.lastname: Pearce
mesh_terms: D001249:Asthma / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D016535:Bronchial Hyperreactivity / Q000276:immunology; D004781:Environmental Exposure / Q000009:adverse effects; D004804:Eosinophils / Q000502:physiology*; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D015848:Interleukin-5 / Q000502:physiology; D016209:Interleukin-8 / Q000502:physiology; D009784:Occupational Diseases / Q000209:etiology
chemical_list: D015848:Interleukin-5; D016209:Interleukin-8