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Review
. 2005 Jun;32(6):483-9.
doi: 10.1165/rcmb.F300.

A centennial history of research on asthma pathogenesis

Michael J Walter  1 , Michael J Holtzman
Affiliations
Review

A centennial history of research on asthma pathogenesis

Michael J Walter et al. Am J Respir Cell Mol Biol. 2005 Jun.
No abstract available

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Figures

<b>Figure 1.</b>
Figure 1.
Evolution of asthma paradigms. Schemes for asthma pathogenesis have ranged from bronchoconstrictor, neurogenic, allergic, inflammatory, and mediator (top panel) as outlined in the text. A current paradigm (bottom panel) attempts to incorporate abnormalities in airway epithelial behavior, antiviral response, and allergic predisposition for the role of the airway immune response in the development of the asthma phenotype. The bottom left panel illustrates how increases in Th1-like antiviral signals (e.g., Stat1 activation and IL-12 p80 expression) in epithelial cells and allergen-driven production of Th2 cytokines (e.g., IL-4, IL-5, IL-9, and IL-13) in immune cells are characteristic of subjects with asthma (designated as an “A”) studied under stable conditions. The bottom right panel illustrates how further increases in epithelial signaling (driven by viral infection) or Th2 cytokine production (driven by further allergen exposure) may develop in subjects with asthma during a flare induced by natural stimuli or by withdrawal from glucocorticoid treatment. In addition, the underlying development of chronically abnormal cellular behavior may depend on respiratory viral infection (and perhaps other environmental stimuli) and a subsequent host response determined by specific genetic programming. The combination of epithelial, viral, and allergic components (as well as the epigenetic characteristics of the process) led to designation of this pathogenesis scheme as an Epi-vir-all paradigm. Modified from Ref. 73.
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