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嗜酸性粒细胞性食管炎的小鼠模型:分子与转化研究见解

Mouse models of eosinophilic esophagitis: molecular and translational insights.

作者信息

Jackson Jazmyne L, Staub Abigail J, Fuller Annie D, Crespo John M, Bordner Travis H, Worrell Courtney, Shanas No'ad, Waheed Danielle, Karakasheva Tatiana A, Ruffner Melanie, Muir Amanda B, Whelan Kelly A

机构信息

Fels Cancer Institute for Personalized Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania, United States.

Department of Biology, Washington & Jefferson College, Washington, Pennsylvania, United States.

出版信息

Am J Physiol Gastrointest Liver Physiol. 2025 Jul 1;329(1):G215-G231. doi: 10.1152/ajpgi.00396.2024. Epub 2025 Jun 3.

DOI:10.1152/ajpgi.00396.2024
PMID:40459956
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12302702/
Abstract

Eosinophilic esophagitis (EoE) is a chronic allergic inflammatory disease of the esophagus that exerts a significant clinical and financial burden in developed countries. Despite an emerging interest in this disease, the cellular and molecular mechanisms driving EoE pathogenesis remain elusive. Addressing this knowledge gap is critical to guide the development of novel approaches for diagnosis, monitoring, and therapy in patients with EoE. As EoE is an allergic inflammatory disorder that results in esophageal inflammation and tissue remodeling, in vivo studies are critical to develop a better understanding of this disease. Here, we provide a review of murine models of EoE, highlighting the mechanistic and translational insights into EoE pathogenesis and therapeutic approaches that studies using these models have uncovered. We further discuss the strengths and limitations of EoE mouse models, as well as opportunities for future in vivo approaches to study EoE. Overall, this article reviews the progress, challenges, unmet needs, and opportunities in murine modeling of EoE.

摘要

嗜酸性食管炎(EoE)是一种食管慢性过敏性炎症性疾病,在发达国家造成了重大的临床和经济负担。尽管对这种疾病的兴趣日益浓厚,但驱动EoE发病机制的细胞和分子机制仍不清楚。填补这一知识空白对于指导EoE患者诊断、监测和治疗新方法的开发至关重要。由于EoE是一种导致食管炎症和组织重塑的过敏性炎症性疾病,体内研究对于更好地理解这种疾病至关重要。在这里,我们对EoE小鼠模型进行综述,强调使用这些模型的研究所揭示的关于EoE发病机制和治疗方法的机制性和转化性见解。我们进一步讨论EoE小鼠模型的优势和局限性,以及未来研究EoE的体内方法的机会。总体而言,本文综述了EoE小鼠建模的进展、挑战、未满足的需求和机会。

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Mouse models of eosinophilic esophagitis: molecular and translational insights.嗜酸性粒细胞性食管炎的小鼠模型:分子与转化研究见解
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本文引用的文献

1
Esophageal epithelial Ikkβ deletion promotes eosinophilic esophagitis in experimental allergy mouse model.食管上皮Ikkβ缺失在实验性变应性小鼠模型中促进嗜酸性食管炎。
J Allergy Clin Immunol. 2025 Apr;155(4):1276-1289. doi: 10.1016/j.jaci.2024.12.1070. Epub 2024 Dec 24.
2
Disease Burden and Spectrum of Symptoms that Impact Quality of Life in Pediatric Patients with Eosinophilic Esophagitis.嗜酸性粒细胞性食管炎患儿的疾病负担及影响生活质量的症状谱
Gastro Hep Adv. 2024 Aug 22;3(8):1054-1068. doi: 10.1016/j.gastha.2024.08.009. eCollection 2024.
3
Prevalence and Costs of Eosinophilic Esophagitis in the United States.
美国嗜酸性粒细胞性食管炎的患病率及成本
Clin Gastroenterol Hepatol. 2025 Feb;23(2):272-280.e8. doi: 10.1016/j.cgh.2024.09.031. Epub 2024 Oct 31.
4
Tissue-specific inducible IL-33 expression elicits features of eosinophilic esophagitis.组织特异性诱导性白细胞介素-33表达引发嗜酸性粒细胞性食管炎的特征。
J Allergy Clin Immunol. 2024 Dec;154(6):1545-1553.e2. doi: 10.1016/j.jaci.2024.08.026. Epub 2024 Sep 10.
5
Amphiregulin-producing T2 cells facilitate esophageal fibrosis of eosinophilic esophagitis.产生双调蛋白的T2细胞促进嗜酸性食管炎的食管纤维化。
J Allergy Clin Immunol Glob. 2024 Jun 4;3(3):100287. doi: 10.1016/j.jacig.2024.100287. eCollection 2024 Aug.
6
Epithelial overexpression of IL-33 induces eosinophilic esophagitis dependent on IL-13.上皮细胞中 IL-33 的过度表达依赖于 IL-13 诱导嗜酸性食管炎。
J Allergy Clin Immunol. 2024 May;153(5):1355-1368. doi: 10.1016/j.jaci.2024.01.017. Epub 2024 Feb 3.
7
A unique role for IL-13 in inducing esophageal eosinophilia through MID-1 and STAT6.白细胞介素-13通过MID-1和信号转导及转录激活因子6在诱导食管嗜酸性粒细胞增多中发挥独特作用。
Front Allergy. 2023 Nov 6;4:1248432. doi: 10.3389/falgy.2023.1248432. eCollection 2023.
8
Real-World Efficacy of Dupilumab in Severe, Treatment-Refractory, and Fibrostenotic Patients With Eosinophilic Esophagitis.真实世界中度利尤单抗治疗重度、难治性、纤维化狭窄性嗜酸性粒细胞性食管炎患者的疗效。
Clin Gastroenterol Hepatol. 2024 Feb;22(2):252-258. doi: 10.1016/j.cgh.2023.08.015. Epub 2023 Sep 3.
9
IL-13-induced STAT3-dependent signaling networks regulate esophageal epithelial proliferation in eosinophilic esophagitis.IL-13 诱导的 STAT3 依赖性信号网络调节嗜酸性粒细胞性食管炎中的食管上皮细胞增殖。
J Allergy Clin Immunol. 2023 Dec;152(6):1550-1568. doi: 10.1016/j.jaci.2023.07.021. Epub 2023 Aug 29.
10
Stem cell factor inhibition reduces Th2 inflammation and cellular infiltration in a mouse model of eosinophilic esophagitis.干细胞因子抑制可减少嗜酸性食管炎小鼠模型中的 Th2 炎症和细胞浸润。
Mucosal Immunol. 2023 Oct;16(5):727-739. doi: 10.1016/j.mucimm.2023.07.006. Epub 2023 Aug 21.