Airway inflammation and asthma.
Asthma is currently identified by the presence of characteristic symptoms of wheezing, chest tightness, dyspnea and cough, and by the presence of reversible airway narrowing and/or airway hyperresponsiveness to a variety of inhaled bronchoconstrictor stimuli. Airway inflammation appears to be central to the pathogenesis of all of these clinical manifestations of asthma. There are increased numbers of activated eosinophils and of mast cells in the airways of patients with asthma, even those with mild disease. The presence and survival of these inflammatory cells may be promoted by the presence of increased levels of proinflammatory cytokines, such as GM-CSF, interleukin(IL)-3 or IL-5 in asthmatic airways. These cells have the capacity to release potent bronchoconstrictor mediators such as the cysteinyl leukotrienes, which are responsible, in part at least, for airway narrowing in asthma and for allergen-g exercise- and aspirin-induced asthma. Other cells, such as a subset of T-lymphocytes (TH2), may also be important in maintaining the inflammatory cascade through the formation and release of cytokines. Airway structural changes caused by the persisting inflammation, such as airway epithelial damage, or altered smooth muscle function or volume, are likely to be important in the pathogenesis of stable long-standing airway hyperresponsiveness. Mediators released from the inflammatory cells may be responsible for these changes. Despite the great increase in knowledge about the importance of airway inflammation in the pathogenesis of asthma, the precise sequence of events that leads to the presence of persisting airway inflammatory cells, airway structural changes and airway hyperresponsiveness in asthma remains to be clarified.
O'Byrne
P M
PM
Department of Medicine, McMaster University, Hamilton, Ontario, Canada.
D001249:Asthma / Q000209:etiology / Q000473:pathology*; D001991:Bronchitis / Q000209:etiology / Q000473:pathology*; D016084:Bronchoconstriction; D006801:Humans; D014136:Tracheitis / Q000209:etiology / Q000473:pathology*