PM2.5 Stimulates Macrophage-Derived Thymic Stromal Lymphopoietin (TSLP) to Induce a Mouse Model of Allergic Conjunctivitis.

IF 1.7 4区 医学 Q3 OPHTHALMOLOGY
Yazhou Qin, Yue Bian, Jingbo Hu, Yuyao Qu, Ruoying Liu, Jixian Ma, Jingming Li, Bo Ma, Cheng Pei, Ning Gao
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引用次数: 0

Abstract

Purpose: Increasing epidemiologic evidence has indicated that PM2.5 exposure is strongly correlated with the prevalence of allergic conjunctivitis (AC), but there is no experimental model for elucidating the underlying mechanism involved. We established a stable PM2.5-induced mouse model of AC to explore the adverse effects of PM2.5 on the ocular surfaces and the underlying mechanisms involved.

Methods: BALB/c mice were sensitized by intraplanar injection of 200 μg PM2.5 on day 0 and challenged for 10 consecutive days, beginning on day 9, with eye drops containing 12.5 mg/mL PM2.5. Assessments of the ocular surfaces, eye blink counts, and tear secretion were performed to evaluate clinical symptoms. The whole eyes were harvested for histopathological and immunofluorescence analyses, the conjunctiva was isolated for Western blotting, and the sera were subjected to IgE ELISA to evaluate the immune characteristics and TSLP-related pathway expression. Furthermore, mouse bone marrow-derived macrophages (BMDMs) were incubated with 25 μg/mL PM2.5 for 24 h. Cellular protein and RNA were extracted for Western blotting and RNA sequencing.

Results: PM2.5 exposure induced clinical manifestations and pathological changes similar to those in human AC. The sensitization and challenge evoked Th2 responses and serum IgE production. PM2.5 exposure mediated TSLP production in macrophages and aggravated allergic inflammation through the TSLP-TSLPR and TSLP-OX40L signaling pathways in vivo. Macrophages produced TSLP and polarized to the M1 phenotype after PM2.5 administration in vitro.

Conclusions: These results demonstrate a reproducible method for establishing a PM2.5-induced AC model. In addition, PM2.5 exposure stimulated macrophages to secrete TSLP and enhance allergic inflammation.

PM2.5刺激巨噬细胞来源的胸腺基质淋巴生成素(TSLP)诱导小鼠过敏性结膜炎模型
目的:越来越多的流行病学证据表明,PM2.5暴露与过敏性结膜炎(AC)的发病率密切相关,但目前还没有实验模型来阐明其中的内在机制。我们建立了一个稳定的PM2.5诱导的小鼠过敏性结膜炎模型,以探讨PM2.5对眼表的不良影响及其内在机制:方法:在第0天向BALB/c小鼠平面内注射200微克PM2.5使其致敏,并从第9天开始连续10天用含12.5毫克/毫升PM2.5的眼药水滴眼。对眼表、眨眼次数和泪液分泌进行评估,以评价临床症状。采集全眼进行组织病理学和免疫荧光分析,分离结膜进行Western印迹分析,并对血清进行IgE ELISA分析,以评估免疫特征和TSLP相关途径的表达。此外,将小鼠骨髓衍生巨噬细胞(BMDMs)与25微克/毫升的PM2.5培养24小时,提取细胞蛋白和RNA进行Western印迹和RNA测序:结果:暴露于PM2.5诱发的临床表现和病理变化与人类AC相似。致敏和挑战诱发 Th2 反应和血清 IgE 生成。PM2.5 暴露介导巨噬细胞产生 TSLP,并通过 TSLP-TSLPR 和 TSLP-OX40L 信号通路加剧体内过敏性炎症。体外给药 PM2.5 后,巨噬细胞产生 TSLP 并极化为 M1 表型:这些结果证明了建立PM2.5诱导的AC模型的可重复性方法。此外,PM2.5 暴露刺激巨噬细胞分泌 TSLP 并增强过敏性炎症。
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来源期刊
Current Eye Research
Current Eye Research 医学-眼科学
CiteScore
4.60
自引率
0.00%
发文量
163
审稿时长
12 months
期刊介绍: The principal aim of Current Eye Research is to provide rapid publication of full papers, short communications and mini-reviews, all high quality. Current Eye Research publishes articles encompassing all the areas of eye research. Subject areas include the following: clinical research, anatomy, physiology, biophysics, biochemistry, pharmacology, developmental biology, microbiology and immunology.
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