ヨシダ　マサキ   Masaki YOSHIDA   吉田　雅紀    所属   応用生物学部 応用生物学科    職種   教授
言語種別	英語
発行・発表の年月	2022/11
形態種別	学術論文
査読	査読あり
標題	Inflammatory Response Induced in Pulmonary Embolic Lung: Evaluation Using a Reproducible Murine Pulmonary Embolism Model
執筆形態	共著
掲載誌名	Global Journal of Biology, Agriculture & Health Sciences
掲載区分	国外
出版社・発行元	Walsh Medical Media
巻・号・頁	11(5),pp.146
著者・共著者	Honoka Okabe, Haruka Kato, Momoka Yoshida, Mayu Kotake, Ruriko Tanabe, Yasuki Matano, Masaki Yoshida, Shintaro Nomura, Atsushi Yamashita, Nobuo Nagai
概要	Background: To assess the pathophysiological response in pulmonary embolism, we established a novel model using a certain volume of relatively small thrombi in mice. Methods: Thrombi with a maximum diameter of 100 µm or 500 Goudy Old Stylem were administered intravenously under anesthesia, and the survival ratio was evaluated at 4 hours. The thrombus location, hemodynamics and Computed Tomography (CT) angiography was assessed after thrombus administration. In addition, quantification of cytokine mRNAs and immunohistochemical analysis for interleukin (IL)-6 and CD68 as a macrophage marker were also performed in normal and embolized lungs at 4 hours. Results: Mice with 100 µm clots showed a dose-dependent survival between 2.3 µL/g and 3.0 µL/g 4 hours after embolization. The thrombi were located at the peripheral region of the lung, which was consistent with the disruption of blood circulation. In CT angiography analysis, approximately 60% of vessels with a diameter of less than 100 µm was occluded in these mice. IL-6 and tumor necrosis factor alpha mRNA were significantly higher and lower, respectively, in embolized lungs than in normal lungs at 4 hours. In both the normal and embolized lungs, IL-6 was expressed in CD68-positive macrophages, and their numbers were comparable. Conclusion: These results show that the pulmonary embolism model induced by a certain amount of small clot is highly reproducible and useful for evaluating pathophysiological responses in the embolized lung. Furthermore, it was found that inflammatory responses shown by IL-6 increase may contribute to the pathogenesis in early stage of pulmonary embolism.