| Autor: |
Yinhui Zeng, MD, Qingxiang Zeng, MD, PhD, Yueqiang Wen, MD, PhD, Jinyuan Li, MD, Haiqing Xiao, MD, Chao Yang, MD, Renzhong Luo, MD, Wenlong Liu, MD, PhD |
| Jazyk: |
angličtina |
| Rok vydání: |
2024 |
| Předmět: |
|
| Zdroj: |
Journal of Allergy and Clinical Immunology: Global, Vol 3, Iss 2, Pp 100212- (2024) |
| Druh dokumentu: |
article |
| ISSN: |
2772-8293 |
| DOI: |
10.1016/j.jacig.2024.100212 |
| Popis: |
Background: Group 2 innate lymphoid cells (ILC2s) have been found to take part in type 2 inflammation by secreting TH2 cytokines. Apolipoprotein A-I (Apo-AI), a major structural and functional protein of high-density lipoproteins, has anti-inflammatory effects on neutrophils, monocytes, macrophages, and eosinophils. However, its effects on ILC2s are not well characterized. Objective: We aimed to investigate the effect of Apo-AI on the proliferation and function of ILC2s as well as its possible mechanism. Methods: The protein expression of Apo-AI and the percentage of ILC2s in peripheral blood between 20 allergic rhinitis patients and 20 controls were detected by ELISA and flow cytometry. The effect of Apo-AI and miR-155 on ILC2 proliferation and function was detected by tritiated thymidine incorporation and ELISA. Anima models were adopted to verify the effect of Apo-AI in vivo. Results: Elevated expression of Apo-AI was observed in allergic rhinitis patients. Apo-AI promotes ABCA1 expression by ILC2s, which can be inhibited by anti–Apo-AI. Apo-AI decreased ILC2 proliferation and the microRNA levels of GATA3 and RORα from ILC2s. The miR-155 overexpression promoted the upregulation of GATA3 and type II cytokines from ILC2s, while the addition of Apo-AI or miR-155 inhibitor significantly inhibited expression of GATA3 and type II cytokines by ILC2s. Apo-AI−/− mice showed as enhanced allergen-induced airway inflammation. The miR-155 inhibitor can reverse the enhanced allergen-induced airway inflammation in Apo-AI−/− mice, while miR-155 mimics can reverse the decreased allergen-induced airway inflammation in Apo-AI–treated mice. Conclusion: Apo-AI suppressed the proliferation and function of ILC2s through miR-155 in allergic rhinitis. Our data provide new insights into the mechanism of allergen-induced airway inflammation. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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