Author Affiliation: Respiratory Cell and Molecular Biology Division, School of Medicine, University of Southampton, Southampton, England.
During the 140 years that followed Henry Hyde Salter's first description
of asthma1 as a distinct syndrome characterized
by paroxysmal episodes of bronchospasm, there has been a relentless search
to understand the mechanisms by which this disease affects the conducting
airways. The specific airway inflammation in asthma involves mast cells, macrophages,
and eosinophils orchestrated by cytokines secreted from a subset of T cells
(TH2-like) and is accompanied by increased bronchial hyperresponsiveness
to both direct (eg, methacholine) and indirect (eg, exercise) stimuli. These
characteristics may in part explain the disordered airway function in asthma,
its relationship to environmental exposures, and therapeutic responses observed
with inhaled corticosteroids and β2-agonists.2,3
For both inhaled corticosteroids and β2-agonists, the last
2 decades have witnessed a progressive improvement in drug efficacy, delivery,
duration of action, and therapeutic index, making twice daily inhaled therapy
for asthma feasible.
Holgate ST. Therapeutic Options for Persistent Asthma. JAMA. 2001;285(20):2637–2639. doi:10.1001/jama.285.20.2637
* * SCHEDULED MAINTENANCE * *
The JAMA Network Sites will be conducting routine maintenance from 10/20/2017 through 10/21/2017. During this window access to content and authentication may be intermittently available. The JAMA Store will be completely unavailable during the maintenance window.