title: Asthma.
abstract: Asthma is the most common inflammatory disease of the lungs. The prevalence of asthma is increasing in many parts of the world that have adopted aspects of the Western lifestyle, and the disease poses a substantial global health and economic burden. Asthma involves both the large-conducting and the small-conducting airways, and is characterized by a combination of inflammation and structural remodelling that might begin in utero. Disease progression occurs in the context of a developmental background in which the postnatal acquisition of asthma is strongly linked with allergic sensitization. Most asthma cases follow a variable course, involving viral-induced wheezing and allergen sensitization, that is associated with various underlying mechanisms (or endotypes) that can differ between individuals. Each set of endotypes, in turn, produces specific asthma characteristics that evolve across the lifecourse of the patient. Strong genetic and environmental drivers of asthma interconnect through novel epigenetic mechanisms that operate prenatally and throughout childhood. Asthma can spontaneously remit or begin de novo in adulthood, and the factors that lead to the emergence and regression of asthma, irrespective of age, are poorly understood. Nonetheless, there is mounting evidence that supports a primary role for structural changes in the airways with asthma acquisition, on which altered innate immune mechanisms and microbiota interactions are superimposed. On the basis of the identification of new causative pathways, the subphenotyping of asthma across the lifecourse of patients is paving the way for more-personalized and precise pathway-specific approaches for the prevention and treatment of asthma, creating the real possibility of total prevention and cure for this chronic inflammatory disease.
authors.affiliation: Clinical and Experimental Sciences, Mail Point 810, Level F, Sir Henry Wellcome Building, Southampton General Hospital, Southampton, SO16 6YD, UK.
authors.forename: Stephen T
authors.initials: ST
authors.lastname: Holgate
authors.affiliation: Subsection Chief of Allergy, Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh, Asthma Institute at UPMC/UPSOM, Pittsburgh, Pennsylvania, USA.
authors.forename: Sally
authors.initials: S
authors.lastname: Wenzel
authors.affiliation: University of Groningen, University Medical Center Groningen, Department of Pulmonology, Groningen, the Netherlands.
authors.forename: Dirkje S
authors.initials: DS
authors.lastname: Postma
authors.affiliation: Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
authors.forename: Scott T
authors.initials: ST
authors.lastname: Weiss
authors.affiliation: Institute of Laboratory Medicine and Pathobiochemistry, Molecular Diagnostics, Philipps University Marburg, University Hospital Giessen and Marburg GmbH, Campus Marburg, Marburg, Germany.
authors.forename: Harald
authors.initials: H
authors.lastname: Renz
authors.affiliation: Queensland Children's Medical Research Institute and Centre for Child Health Research, University of Queensland, Brisbane, Australia.
authors.forename: Peter D
authors.initials: PD
authors.lastname: Sly
mesh_terms: D000485:Allergens / Q000009:adverse effects; D001249:Asthma / Q000209:etiology; D018450:Disease Progression; D044127:Epigenesis, Genetic; D006801:Humans; D006967:Hypersensitivity / Q000150:complications; D010641:Phenotype; D012135:Respiratory Sounds / Q000209:etiology
chemical_list: D000485:Allergens