Figures
- FIGURE 1
Two different pathways lead to eosinophilic airway inflammation in asthma. In allergic asthma, dendritic cells present allergens to CD4+ T-cells, inducing T-helper (Th)2 cells, which produce interleukin (IL)-4, IL-5 and IL-13, and leading to IgE switching in B-cells, airway eosinophilia and mucous hypersecretion. In nonallergic eosinophilic asthma, air pollutants, microbes and glycolipids induce the release of epithelium-derived cytokines, including IL-33, IL-25 and thymic stromal lymphopoietin (TSLP), which activate innate lymphoid cells (ILCs) in an antigen-independent manner via their respective receptors (IL-17 receptor B (IL-17RB), ST2 and TSLP receptor (TSLPR)). Activated ILC2s produce high amounts of IL-5 and IL-13, leading to eosinophilia, mucus hypersecretion and airway hyperreactivity. CRTH2: chemoattractant receptor homologous molecule expressed on Th2 cells; ALX/FPR2: receptor for lipoxin A4; FcεRI: high-affinity receptor for IgE; GATA3: GATA-binding protein 3; PG: prostaglandin; ROR: retinoic acid receptor-related orphan receptor; NK: natural killer; MHC: major histocompatibility complex; TCR: T-cell receptor. Reproduced from [51] with permission from the publisher.
- FIGURE 2
Effect of high dose triamcinolone on sputum eosinophils. Effect of treatment with intramuscular triamcinolone or placebo on sputum eosinophil percentages in 22 patients with eosinophilic asthma. Horizontal lines represent median values. Reproduced and modified from [87] with permission from the publisher.
Tables
- TABLE 1
Clinical profile of late-onset eosinophilic asthma patients
Adult onset of asthma Equal distribution between sexes Few or no allergies to common allergens Elevated eosinophils in peripheral blood At risk of severe exacerbations Normal or moderately elevated IgE level Low FEV1 and often persistent airflow limitation Air trapping and dynamic hyperinflation Chronic rhinosinusitis with nasal polyposis Aspirin sensitivity Good response to systemic corticosteroids Good response to anti IL-5 treatment FEV1: forced expiratory volume in 1 s; IL: interleukin.
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- Article
- Abstract
- Abstract
- Introduction
- Asthma phenotypes and the role of the eosinophil
- Molecular pathways of eosinophilic inflammation
- Clinical profile of the patient with eosinophilic asthma
- Management of the patient with eosinophilic asthma
- New treatment options for the patient with eosinophilic asthma
- Conclusions
- Footnotes
- References
- Figures & Data
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