Endotypes of severe allergic asthma patients who clinically benefit from anti‐IgE therapy. Issue 1 (11th September 2018)

• Record Type: Journal Article
• Authors: Huang, Yu‐Chen; Weng, Chih‐Ming; Lee, Meng‐Jung; Lin, Shu‐Min; Wang, Chun‐Hua; Kuo, Han‐Pin
• Is Part Of: Clinical & experimental allergy. Volume 49:Issue 1(2019)
• Page Start: 44
• Page End: 53
• Publication Date: 2018-09-11
• Subjects: anti‐IgE -- IgE -- IL‐25 -- IL‐33 -- severe asthma -- thymic stromal lymphopoietin -- type 2 cytokines; Allergy -- Periodicals; Immunology -- Periodicals; 616.97
• DOI: 10.1111/cea.13248
• Languages: English
• ISSNs: 0954-7894

Abstract

Summary: Background: Omalizumab, a recombinant monoclonal anti‐IgE antibody, was developed for the treatment of severe allergic asthma. Not all these patients respond to omalizumab. Objective: This study aimed to evaluate whether the proinflammatory cytokine profiles in the severe allergic asthma patients were different between who responded and nonresponded to omalizumab therapy. Methods: A prospective study was conducted to examine type 2 cytokines and epithelium‐derived cytokines in the bronchial tissues by immunohistochemistry, Western blot and PCR analysis among patients with severe allergic asthma before and after omalizumab therapy. Results: Fourteen of 23 patients with unstable severe allergic asthma improved their asthma control after 4 months of omalizumab treatment (Responders), while nine failed to improve (Non‐Responders). Most of Responders were type 2‐high endotype (12/14) with upregulated expression of IL‐33, IL‐25 and TSLP in their bronchial tissues, while most of Non‐Responders were type 2‐low endotype (8/9). Repeated bronchoscopic biopsy was done in nine responders after omalizumab treatment and showed a decline in IL‐13, IL‐33, IL‐25 and TSLP expression in the bronchial tissues. Among 14 Responders who continued omalizuamb treatments to a total 12 months, six patients achieved a well control of asthma (ACT ≥ 23), while eight patients required additional treatment for asthma symptoms and had more rhinosinusitis comorbidities and a mixed eosinophilic and neutrophilic inflammation in their bronchial tissues. Conclusion: Most of the severe allergic asthma patients who benefited from omalizumab treatment were IL‐33, IL‐25 and TSLP aggravated type 2‐high endotype. Rhinosinusitis or with a mixed eosinophilic and neutrophilic airway inflammation should be evaluated in patients who partially responded to omalizumab treatment.