دورية أكاديمية
Deficiency of interleukin-6 receptor ameliorates PM2.5 exposure-induced pulmonary dysfunction and inflammation but not abnormalities in glucose homeostasis
| العنوان: | Deficiency of interleukin-6 receptor ameliorates PM2.5 exposure-induced pulmonary dysfunction and inflammation but not abnormalities in glucose homeostasis |
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| المؤلفون: | Renzhen Peng, Wenhui Yang, Wenpu Shao, Bin Pan, Yaning Zhu, Yubin Zhang, Haidong Kan, Yanyi Xu, Zhekang Ying |
| المصدر: | Ecotoxicology and Environmental Safety, Vol 247, Iss , Pp 114253- (2022) |
| بيانات النشر: | Elsevier, 2022. |
| سنة النشر: | 2022 |
| المجموعة: | LCC:Environmental pollution LCC:Environmental sciences |
| مصطلحات موضوعية: | PM2.5, IL-6R, Inflammation, Pulmonary dysfunction, Glucose homeostasis, Environmental pollution, TD172-193.5, Environmental sciences, GE1-350 |
| الوصف: | Background: Ambient fine particulate matter (PM2.5) exposure increases local and systemic interleukin-6 (IL-6). However, the pathogenic role of IL-6 signalling following PM2.5 exposure, particularly in the development of pulmonary dysfunction and abnormal glucose homeostasis, has hardly been investigated. Results: In the study, IL-6 receptor (IL-6R)-deficient (IL-6R-/-) and wildtype littermate (IL-6R+/+) mice were exposed to concentrated ambient PM2.5 (CAP) or filtered air (FA), and their pulmonary and metabolic responses to these exposures were analyzed. Our results demonstrated that IL-6R deficiency markedly alleviated PM2.5 exposure-induced increases in lung inflammatory markers including the inflammation score of histological analysis, the number of macrophages in bronchoalveolar lavage fluid (BALF), and mRNA expressions of TNFα, IL-1β and IL-6 and abnormalities in lung function test. However, IL-6R deficiency did not reduce the hepatic insulin resistance nor systemic glucose intolerance and insulin resistance induced by PM2.5 exposure. Conclusion: Our findings support the crucial role of IL-6 signalling in the development of pulmonary inflammation and dysfunction due to PM2.5 exposure but question the putative central role of pulmonary inflammation for the extra-pulmonary dysfunctions following PM2.5 exposure, providing a deep mechanistic insight into the pathogenesis caused by PM2.5 exposure. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 0147-6513 |
| Relation: | http://www.sciencedirect.com/science/article/pii/S0147651322010934; https://doaj.org/toc/0147-6513 |
| DOI: | 10.1016/j.ecoenv.2022.114253 |
| URL الوصول: | https://doaj.org/article/cafdb987c82c4159b1c27d2081bec9c0 |
| رقم الأكسشن: | edsdoj.fdb987c82c4159b1c27d2081bec9c0 |
| قاعدة البيانات: | Directory of Open Access Journals |
Full Text Finder | تدمد: | 01476513 |
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| DOI: | 10.1016/j.ecoenv.2022.114253 |