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粒细胞集落刺激因子增强的红细胞动员与小鼠中炭疽致死毒素诱导的死亡率降低有关。

Erythrocytic mobilization enhanced by the granulocyte colony-stimulating factor is associated with reduced anthrax-lethal-toxin-induced mortality in mice.

作者信息

Chang Hsin-Hou, Chiang Ya-Wen, Lin Ting-Kai, Lin Guan-Ling, Lin You-Yen, Kau Jyh-Hwa, Huang Hsin-Hsien, Hsu Hui-Ling, Wang Jen-Hung, Sun Der-Shan

机构信息

Department of Molecular Biology and Human Genetics, Tzu-Chi University, Hualien, Taiwan; Institute of Medical Sciences, Tzu-Chi University, Hualien, Taiwan.

Department of Molecular Biology and Human Genetics, Tzu-Chi University, Hualien, Taiwan.

出版信息

PLoS One. 2014 Nov 10;9(11):e111149. doi: 10.1371/journal.pone.0111149. eCollection 2014.

Abstract

Anthrax lethal toxin (LT), one of the primary virulence factors of Bacillus anthracis, causes anthrax-like symptoms and death in animals. Experiments have indicated that levels of erythrocytopenia and hypoxic stress are associated with disease severity after administering LT. In this study, the granulocyte colony-stimulating factor (G-CSF) was used as a therapeutic agent to ameliorate anthrax-LT- and spore-induced mortality in C57BL/6J mice. We demonstrated that G-CSF promoted the mobilization of mature erythrocytes to peripheral blood, resulting in a significantly faster recovery from erythrocytopenia. In addition, combined treatment using G-CSF and erythropoietin tended to ameliorate B. anthracis-spore-elicited mortality in mice. Although specific treatments against LT-mediated pathogenesis remain elusive, these results may be useful in developing feasible strategies to treat anthrax.

摘要

炭疽致死毒素(LT)是炭疽芽孢杆菌的主要毒力因子之一,可在动物身上引发类似炭疽的症状并导致死亡。实验表明,在给予LT后,红细胞减少和缺氧应激水平与疾病严重程度相关。在本研究中,粒细胞集落刺激因子(G-CSF)被用作治疗剂,以改善C57BL/6J小鼠因炭疽-LT和孢子诱导的死亡率。我们证明,G-CSF促进成熟红细胞向外周血的动员,从而使红细胞减少症的恢复明显加快。此外,使用G-CSF和促红细胞生成素的联合治疗倾向于改善小鼠中炭疽芽孢杆菌孢子引发的死亡率。尽管针对LT介导的发病机制的具体治疗方法仍不明确,但这些结果可能有助于制定可行的炭疽治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8ad/4226491/d0bcd3b7238a/pone.0111149.g001.jpg

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