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Review
. 2010 Aug;138(2 Suppl):4S-10S.
doi: 10.1378/chest.10-0100.

The relationship of airway hyperresponsiveness and airway inflammation: Airway hyperresponsiveness in asthma: its measurement and clinical significance

William W Busse  1
Affiliations
Review

The relationship of airway hyperresponsiveness and airway inflammation: Airway hyperresponsiveness in asthma: its measurement and clinical significance

William W Busse. Chest. 2010 Aug.

Abstract

Airway hyperresponsiveness (AHR) is a clinical feature of asthma and is often in proportion to the underlying severity of the disease. To understand AHR and the mechanisms that contribute to these processes, it is helpful to divide the airway components that affect this feature of asthma into "persistent" and "variable" categories. The persistent component of AHR represents structural changes in the airway, whereas the variable feature relates to inflammatory events. Insight into how these interrelated components of AHR can contribute to asthma is gained by studying treatment effects and models of asthma provocation.

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Figures

Figure 1.
Figure 1.
Dose-response curves to inhaled direct agonists (histamine or methacholine) in normal, mild, or severe asthma. (Reprinted with permission from O’Byrne et al.)
Figure 2.
Figure 2.
Components of airway changes in asthma that contribute to AHR. AHR = airway hyperresponsiveness.
Figure 3.
Figure 3.
Factors affecting the variable and persistent components of AHR. See Figure 2 legend for an expansion of the abbreviation.
Figure 4.
Figure 4.
Detection of AHR by direct and indirect activators of airway contraction. See Figure 2 legend for expansion of the abbreviation.
Figure 5.
Figure 5.
Individual changes in reticular layer thickness beneath the epithelium in bronchial biopsies before and after 2 years of treatment in reference and AHR strategy. See Figure 2 legend for expansion of abbreviation. (Reprinted with permission from Sont et al.)
Figure 6.
Figure 6.
Relationship between changes in EG2+ eosinophils and changes in methacholine PC20 during 2 years’ treatment in reference and AHR strategy. EG2+ = Monoclonal antibody that binds to eosinophil cationic protein; PC20 = provocative concentration causing a 20% fall in FEV1. See Figure 2 legend for expansion of the other abbreviation. (Reprinted with permission from Sont et al.)
Figure 7.
Figure 7.
Summary of the study design from Kariyawasam et al. V = visit. See Figures 2 and 6 legends for expansion of other abbreviations. (Reprinted with permission from Kariyawasam et al.)
Figure 8.
Figure 8.
The changes from baseline in FEV1 (A) and methacholine (B) 24 h and 7 days after antigen challenge. ns = not significant. (Reprinted with permission from Kariyawasam et al.)
Figure 9.
Figure 9.
Markers of airway remodeling 24 h and 7 days after antigen challenge. (Reprinted with permission from Kariyawasam et al.)
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References

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