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OX40 在嗜酸性粒细胞中的表达加重了 OVA 诱导的嗜酸性粒细胞性胃肠炎。

OX40 Expression in Eosinophils Aggravates OVA-Induced Eosinophilic Gastroenteritis.

机构信息

Department of Gastroenterology, Peking University Ninth School of Clinical Medicine, Beijing, China.

Beijing Key Laboratory of Tolerance Induction and Organ Protection in Transplantation, Beijing, China.

出版信息

Front Immunol. 2022 Jun 2;13:841141. doi: 10.3389/fimmu.2022.841141. eCollection 2022.

DOI:10.3389/fimmu.2022.841141
PMID:35720294
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9201343/
Abstract

BACKGROUND & AIMS: Eosinophils are the main inflammatory effector cells that damage gastrointestinal tissue in eosinophilic gastrointestinal diseases (EGIDs). Activation of the OX40 pathway aggravates allergic diseases, such as asthma, but it is not clear whether OX40 is expressed in eosinophils to regulate inflammation in EGIDs. In this study, we assessed the expression and effect of OX40 on eosinophils in WT and eosinophilic gastroenteritis (EGE) mice.

METHODS

Eosinophil infiltration, ovalbumin (OVA)-specific Ig production, OX40 expression and inflammatory factor levels in the intestine and bone marrow (BM) were investigated to evaluate inflammation.

RESULTS

We confirmed that OVA-challenged mice produced high levels of mRNA and a low level of mRNA in the intestine. Increased eosinophils were observed in intestinal and lymph tissues, accompanied by significantly upregulated OX40 and Type 2 cytokine production in eosinophils of EGE mice. deficiency ameliorated OVA-induced inflammation, eosinophil infiltration, and cytokine production in the intestine. Consistently, eosinophils exhibited decreased proliferation and proinflammatory function. The stimulation of the agonistic anti-OX40 antibody, OX86, promoted the effect of OX40 on eosinophils. The present study also showed that deficiency dampened the Traf2/6-related NF-κB signaling pathway in eosinophils.

CONCLUSIONS

OX40 may play a critical role in the progress of OVA-induced EGE by promoting the maturation and function of eosinophils the Traf2/6-related NF-κB signaling pathway.

摘要

背景与目的

嗜酸性粒细胞是导致胃肠道组织损伤的主要炎症效应细胞，在嗜酸性粒细胞性胃肠道疾病（EGIDs）中发挥作用。OX40 通路的激活会加重哮喘等过敏性疾病，但目前尚不清楚 OX40 是否在嗜酸性粒细胞中表达，以调节 EGIDs 中的炎症。本研究评估了 OX40 在 WT 和嗜酸性粒细胞性胃肠炎（EGE）小鼠中对嗜酸性粒细胞的表达和作用。

方法

通过评估嗜酸性粒细胞浸润、卵清蛋白（OVA）特异性 Ig 产生、OX40 表达和肠道及骨髓（BM）中炎症因子水平，来评估炎症。

结果

我们证实，OVA 挑战的小鼠在肠道中产生高水平的 mRNA 和低水平的 mRNA。在 EGE 小鼠中，观察到肠道和淋巴组织中嗜酸性粒细胞增多，同时伴有 OX40 和 2 型细胞因子在嗜酸性粒细胞中的表达显著上调。缺失减轻了 OVA 诱导的肠道炎症、嗜酸性粒细胞浸润和细胞因子产生。同样，缺失的 嗜酸性粒细胞增殖和促炎功能降低。激动性抗-OX40 抗体 OX86 的刺激促进了 OX40 对嗜酸性粒细胞的作用。本研究还表明，缺失抑制了嗜酸性粒细胞中 Traf2/6 相关 NF-κB 信号通路。

结论

OX40 可能通过促进嗜酸性粒细胞的成熟和功能，在 OVA 诱导的 EGE 进展中发挥关键作用，该作用涉及 Traf2/6 相关 NF-κB 信号通路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eec0/9201343/9a7e2ca53c5d/fimmu-13-841141-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eec0/9201343/5e0386d4a24d/fimmu-13-841141-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eec0/9201343/3adf528b436d/fimmu-13-841141-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eec0/9201343/8493b7dc0911/fimmu-13-841141-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eec0/9201343/9a7e2ca53c5d/fimmu-13-841141-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eec0/9201343/5e0386d4a24d/fimmu-13-841141-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eec0/9201343/23d171ddff21/fimmu-13-841141-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eec0/9201343/d0369bb00678/fimmu-13-841141-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eec0/9201343/24def9d9e10c/fimmu-13-841141-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eec0/9201343/3adf528b436d/fimmu-13-841141-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eec0/9201343/8493b7dc0911/fimmu-13-841141-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eec0/9201343/9a7e2ca53c5d/fimmu-13-841141-g007.jpg

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