Angiotensin converting enzyme 2 activation improves allergic rhinitis and suppresses Th2 cytokine release
Abstract Objective Allergic rhinitis (AR) is primarily regulated by type I hypersensitivity, with Th2 and immunoglobulin E (IgE) playing essential roles. This study aimed to determine whether angiotensin converting enzyme (ACE)2 could participate in the regulation of AR. Methods Nasal mucosal tissue...
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| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
2023-01-01
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| Series: | Immunity, Inflammation and Disease |
| Subjects: | |
| Online Access: | https://doi.org/10.1002/iid3.763 |
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| Summary: | Abstract Objective Allergic rhinitis (AR) is primarily regulated by type I hypersensitivity, with Th2 and immunoglobulin E (IgE) playing essential roles. This study aimed to determine whether angiotensin converting enzyme (ACE)2 could participate in the regulation of AR. Methods Nasal mucosal tissues of AR patients were collected to determine ACE2 levels. Following AR mouse models were established, ACE2 levels in nasal mucosa were determined. Then the influences of diminazene aceturate (ACE2 agonist) on AR symptoms, pathology, specific antibodies, histamine, and interleukins (ILs) release in vivo were evaluated. Afterward, human nasal mucosa epithelial cells were exposed to IL‐13, and the impacts of ACE2 overexpression on the secretion of pro‐inflammatory factors in vitro were assessed. Results ACE2 levels significantly declined in nasal mucosa both in patients and mouse models (p < .001). Diminazene aceturate treatment elevated the ACE2 level in mice (p < .01), accompanied by reduced frequency of nasal spray and nasal friction, decreased eosinophils and goblet cells (p < .001) according to histopathological staining. Furthermore, lgE, lgG1, histamine, and IL levels in mice were also decreased (p < .05). In vitro experiments revealed that ACE2 overexpression suppressed the secretion of pro‐inflammatory factors (p < .001). Conclusion Together, ACE2 activation can alleviate the symptoms of AR in mice and inhibit the release of Th2 cytokines. Activating ACE2 is a promising therapeutic approach for AR. |
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| ISSN: | 2050-4527 |