1. Airway inflammation in asthma and its consequences: Implications for treatment in children and adults 
Ratko Djukanovic, MD 
Journal of Allergy and Clinical Immunology 
Volume 109, Issue 6, Pages S539-S548 (June 2002)
DOI: /mai
Copyright © 2002 Mosby, Inc. Terms and Conditions

2. Fig. 1
Eosinophilia is a typical feature of mild, steroid-naive asthma, but many patients with severe asthma have few (within the normal range) eosinophils staining positively with the anti-ECP antibody EG2 in their bronchial mucosa (left panel). Severe asthma is typified by infiltration with activated T cells bearing IL-2 receptor (CD25+) on the cell surface, indicating recent activation (right panel). (Adapted with permission from Vrugt B, Wilson S, Underwood J, et al. Mucosal inflammation in severe glucocorticosteroid-dependent asthma. Eur Respir J 1999;13: © European Respiratory Society Journals Ltd.)
Journal of Allergy and Clinical Immunology  , S539-S548DOI: ( /mai )
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3. Fig. 2
When patients with severe, corticosteroid-dependent asthma are divided into those with mucosal eosinophil counts within the normal range (Eos-) and those with elevated counts (Eos+), those with eosinophilia have greater EG2+ cells (left panel) as well as greater CD3+ T cells (right panel) in the airways. In addition, they have greater mast cell activation, as indicated by increased tryptase levels in BAL and increased collagen deposition. (From Wenzel SE, Schwarts LB, Langmack EL, et al. Evidence that severe asthma can be divided pathologically into two inflammatory subtypes with distinct physiologic and clinical characteristics. Am J Respir Crit Care Med 1999;160: Official Journal of the American Thoracic Society. © American Lung Association.)
Journal of Allergy and Clinical Immunology  , S539-S548DOI: ( /mai )
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4. Fig. 3
Asthma severity is broadly related to sputum eosinophilia, although considerable heterogeneity exists within each asthma severity group (left panel). When patients are subdivided according to treatment with ICS or OCS, no significant differences can be seen between the subgroups (right panel). (From Louis R, Lau LC, Bron AO, et al. The relationship between airways inflammation and asthma severity. Am J Respir Crit Care Med 2000;161:9-16. Official Journal of the American Thoracic Society. © American Thoracic Society.)
Journal of Allergy and Clinical Immunology  , S539-S548DOI: ( /mai )
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5. Fig. 4
Correlation between tryptase concentrations in BAL and bronchial responsiveness, as determined by PC20 histamine. Increased tryptase levels correlated with BHR. No correlation was found between BHR and eosinophils. (From Ferguson AC, Whitelaw M, Brown H. Correlation of bronchial eosinophil and mast cell activation with bronchial hyperresponsiveness in children with asthma. J Allergy Clin Immunol 1992;90: With permission.)
Journal of Allergy and Clinical Immunology  , S539-S548DOI: ( /mai )
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6. Fig. 5
Pathogenesis of asthma. Inflammation per se is not sufficient to cause asthma, but the susceptibility of the airway structures to damage by chronic inflammation may be critical. The origin of the susceptibility is unknown but it could be inherited or it could result from injury.
Journal of Allergy and Clinical Immunology  , S539-S548DOI: ( /mai )
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7. Fig. 6
Positive relation between subepithelial collagen deposition and asthma severity is depicted. Signaling by EGF promotes epithelial proliferation and generation of metalloproteinases, whereas signaling by TGF-β receptor inhibits these and enhances collagen deposition.
Journal of Allergy and Clinical Immunology  , S539-S548DOI: ( /mai )
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8. Fig. 7
Extent of subepithelial airway fibrosis in subjects with mild to severe asthma and in normal control subjects. There was a significant increase in airway fibrosis in subjects with severe (***P < .001), moderate (**P < .001), and mild (*P < .005) asthma compared with normal control subjects. (From Minshall EM, Leung, DY, Martin RJ, et al. Eosinophil-associated TGF-beta1 mRNA expression and airways fibrosis in bronchial asthma. Am J Respir Cell Mol Biol 1997;17:l Official Journal of the American Thoracic Society. © American Lung Association.)
Journal of Allergy and Clinical Immunology  , S539-S548DOI: ( /mai )
Copyright © 2002 Mosby, Inc. Terms and Conditions