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环境烟草烟雾对小鼠Th2细胞介导的鼻嗜酸性粒细胞炎症的抑制作用。

Suppressive effect of environmental tobacco smoke on murine Th2 cell-mediated nasal eosinophilic inflammation.

作者信息

Nishimura Tomoe, Kaminuma Osamu, Saeki Mayumi, Kitamura Noriko, Mori Akio, Hiroi Takachika

机构信息

Allergy and Immunology Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.

Clinical Research Center for Allergy and Rheumatology, National Hospital Organization, Sagamihara National Hospital, Kanagawa, Japan.

出版信息

Asia Pac Allergy. 2020 Apr 27;10(2):e18. doi: 10.5415/apallergy.2020.10.e18. eCollection 2020 Apr.

DOI:10.5415/apallergy.2020.10.e18
PMID:32411583
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7203434/
Abstract

BACKGROUND

Environmental tobacco smoke (ETS) exposure is recognized as a risk factor for the development of various respiratory diseases.

OBJECTIVE

In this study, the effect of ETS on allergen-immunized and allergen-specific Th2 cell-transferred murine eosinophilic inflammation models and that of cigarette smoke extract (CSE) and nicotine on allergen-induced Th2 cell proliferation and interleukin (IL)-4 production were investigated.

METHODS

Ovalbumin (OVA)-immunized and OVA-specific Th2 cell-transferred BALB/c mice were exposed to ETS and were challenged with OVA. Then, the number of inflammatory cells in the nasal mucosa and nasal hyperresponsiveness (NHR) were assessed. The effects of CSE and nicotine on the allergen-induced proliferative response of and IL-4 production by Th2 cells were determined .

RESULTS

In OVA-immunized and Th2 cell-transferred mice, allergen-induced NHR and nasal eosinophil infiltration were significantly suppressed by ETS exposure, whereas the accumulation of neutrophils was rather enhanced. Allergen-specific Th2 cell proliferation and IL-4 production were inhibited by coculture with CSE. The same effects were induced by nicotine, though the effect on proliferation was relatively weak.

CONCLUSION

Regardless of its harmful effect, ETS suppresses NHR, probably through the inhibition of Th2 cell responses.

摘要

背景

环境烟草烟雾（ETS）暴露被认为是多种呼吸道疾病发生的危险因素。

目的

在本研究中，研究了ETS对变应原免疫和变应原特异性Th2细胞转移的小鼠嗜酸性粒细胞炎症模型的影响，以及香烟烟雾提取物（CSE）和尼古丁对变应原诱导的Th2细胞增殖和白细胞介素（IL）-4产生的影响。

方法

将卵清蛋白（OVA）免疫和OVA特异性Th2细胞转移的BALB/c小鼠暴露于ETS，并给予OVA激发。然后，评估鼻黏膜中的炎症细胞数量和鼻高反应性（NHR）。测定CSE和尼古丁对变应原诱导的Th2细胞增殖反应和IL-4产生的影响。

结果

在OVA免疫和Th2细胞转移的小鼠中，ETS暴露显著抑制了变应原诱导的NHR和鼻嗜酸性粒细胞浸润，而中性粒细胞的积聚反而增强。与CSE共培养可抑制变应原特异性Th2细胞增殖和IL-4产生。尼古丁也诱导了相同的效应，尽管其对增殖的影响相对较弱。

结论

尽管ETS有有害作用，但它可能通过抑制Th2细胞反应来抑制NHR。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59f7/7203434/4b1afc784389/apa-10-e18-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59f7/7203434/99a2b2933a9c/apa-10-e18-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59f7/7203434/829b09b0041a/apa-10-e18-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59f7/7203434/562bd09409da/apa-10-e18-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59f7/7203434/4b1afc784389/apa-10-e18-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59f7/7203434/99a2b2933a9c/apa-10-e18-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59f7/7203434/829b09b0041a/apa-10-e18-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59f7/7203434/562bd09409da/apa-10-e18-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59f7/7203434/4b1afc784389/apa-10-e18-g004.jpg

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