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瘦素通过 PI3K/AKT 通路调节变应性鼻炎中的 ILC2 细胞。

Leptin Regulated ILC2 Cell through the PI3K/AKT Pathway in Allergic Rhinitis.

机构信息

Department of Otolaryngology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.

出版信息

Mediators Inflamm. 2020 Mar 7;2020:4176082. doi: 10.1155/2020/4176082. eCollection 2020.

DOI:10.1155/2020/4176082
PMID:32214904
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7081033/
Abstract

BACKGROUND

Recent studies suggest that leptin is involved in Th2 response in allergic rhinitis (AR). However, the effect of leptin on type II innate lymphoid cells (ILC2s) in AR is not well characterized.

METHODS

Twenty-six AR patients and 20 healthy controls were enrolled. Serum leptin levels were measured, and their correlation with ILC2 and type II cytokines were analyzed using enzyme-linked immunosorbent assay (ELISA) and flow cytometry. ILC2 differentiation and cytokine production stimulated by human recombinant leptin were analyzed by real-time polymerase chain reaction (PCR) and ELISA. AR mouse models were also established to verify the effect of leptin on ILC2 cell regulation.

RESULTS

Our results showed that elevated serum leptin in AR patients was correlated with the percentage of ILC2 and the expression of type II cytokines. The recombinant leptin enhanced the expression of ILC2 cell transcription factors and type II cytokine through the PI3K/AKT pathway. The AR mice treated with leptin showed as stronger ILC2 inflammation and symptoms compared with control mice.

CONCLUSIONS

Our data provide evidence that upregulation of leptin promotes ILC2 responses in AR and this process was achieved through the PI3K/AKT pathway.

摘要

背景

最近的研究表明,瘦素参与了变应性鼻炎(AR)中的 Th2 反应。然而,瘦素对 AR 中 II 型固有淋巴细胞(ILC2)的影响尚未得到很好的描述。

方法

纳入 26 名 AR 患者和 20 名健康对照者。采用酶联免疫吸附试验(ELISA)和流式细胞术检测血清瘦素水平,并分析其与 ILC2 和 II 型细胞因子的相关性。通过实时聚合酶链反应(PCR)和 ELISA 分析人重组瘦素刺激 ILC2 分化和细胞因子产生的情况。还建立了 AR 小鼠模型以验证瘦素对 ILC2 细胞调节的作用。

结果

我们的结果表明,AR 患者血清瘦素水平升高与 ILC2 的百分比和 II 型细胞因子的表达相关。重组瘦素通过 PI3K/AKT 通路增强了 ILC2 细胞转录因子和 II 型细胞因子的表达。与对照小鼠相比,接受瘦素治疗的 AR 小鼠表现出更强的 ILC2 炎症和症状。

结论

我们的数据提供了证据表明,瘦素的上调促进了 AR 中 ILC2 的反应,这一过程是通过 PI3K/AKT 通路实现的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f867/7081033/20bc581a9d42/MI2020-4176082.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f867/7081033/ca9e7d6154dc/MI2020-4176082.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f867/7081033/15357f8cc48b/MI2020-4176082.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f867/7081033/c894843ea587/MI2020-4176082.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f867/7081033/20bc581a9d42/MI2020-4176082.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f867/7081033/ca9e7d6154dc/MI2020-4176082.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f867/7081033/15357f8cc48b/MI2020-4176082.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f867/7081033/c894843ea587/MI2020-4176082.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f867/7081033/20bc581a9d42/MI2020-4176082.004.jpg

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