IL-17–high asthma with features of a psoriasis immunophenotype

Abstract

U-BIOPRED cohort n=91 epithelial brushings or biopsies IL-17 High Clinical phenotype Nasal polyps Smoking Antibiotic use Epithelial Gene Expression Profile Clinical phenotype FeNO Exacerbations Gene expression shared with psoriasis IDO1 IL1B DEFB4B S100A8, S100A9 PI3 CXCL3, CXCL8 CXCL10, CCL20 Gene signature SERPINB2 POSTN CLCA1 IL-13 High T cell infiltration Neutrophilia Eosinophilia IL-17-high asthma with features of a psoriasis immunophenotype From a the Respiratory,

Review—Current Concepts in Inflammatory Skin Diseases Evolved by Transcriptome Analysis: In-Depth Analysis of Atopic Dermatitis and Psoriasis

“…In allergic asthma, IL-17-and IL-13-driven endotypes aggregated separately in an unsupervised clustering analysis and the two profiles seemed to be exclusive. In addition, this led to the identification of smoking as a risk factor specifically for the IL-17-driven type [190].…”

New Perspectives for Mucolytic, Anti-inflammatory and Adjunctive Therapy with 1,8-Cineole in COPD and Asthma: Review on the New Therapeutic Approach

“…F. These results showed that 1,8-cineole has at least two different pharmacological actions in the same molecule as a bifunctional drug besides it bronchodilatory, antimicrobial and other activities for the treatment of inflammatory airway diseases. Th1-type inflammation in high IL-17 phenotype very often plays a key role in frequently exacerbating neutrophilic asthma and COPD [76], which is also controlled by 1,8-cineole in addition to its control of Th2-type inflammation [33]. In this regard, adjunctive pulse therapies with azithromycin (3 9 500 mg per week) [77] and clarithromycin (2 9 500 mg per week) [78] for 1 year are recommended only for these antibiotics to control exacerbations besides known side effects (evidence A) by the current Task Force Report of the GOLD Executive Summary [4].…”

Involvement of the epidermal growth factor receptor in IL‐13–mediated corticosteroid‐resistant airway inflammation

“…and HB-EGF expression; the other sub-cluster was characterized by 18 showed that EGFR and ERBB2 were significantly downregulated and ERBB3 up-regulated in severe asthmatics with "IL- 13" or "IL-17 high" phenotypes but not in those subjects with an "IL-13/ IL-17 low" phenotype. In contrast, in the latter group, ERBB4 was the only ERBB family member to show significant modulation (Table 1).…”

“…16 Elevated levels of these biomarkers are frequently associated with the presence of atopy and bronchial hyperresponsiveness (BHR) 17 and are considered to be sensitive to inhibition by corticosteroids and monoclonal antibodies against IgE, IL-5 or IL-5 receptor. 1,12,17 In contrast, patients who have "non-Type-2" (also known as "Type-2-low") severe asthma are frequently characterized by airway neutrophilia, a Type-17 immune signature involving genes such as CXCL1, CXCL2 and CSF3 18 and disease that is not effectively treated by inhaled corticosteroids or biologics. 6 While this broad classification of corticosteroid responsiveness in relation to Type-2 inflammation is a reasonable generalization, studies with dupilumab, an antibody to IL-4Rα, suggest it is an over-simplification.…”