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在巨细胞中MAPK/ERK的激活促进了莱什马尼亚内部化和病原体的产生

Umaru Barrie¹, Katherine Floyd², Arani Datta²

¹Department of Pediatrics, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX, 75390, United States; Medical Scientist Training Program, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX, 75390, United States.

Microbes and infection

|May 19, 2024

概括

阻断基激活蛋白/细胞外信号调节激酶 (MAPK/ERK) 途径,可以防止宿主细胞吸收莱什曼尼亚. 这一发现为莱什曼病提供了一种新的治疗策略,减少了疾病的严重程度和寄生虫负担.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学
寄生虫学的寄生虫学

背景情况:

莱什曼尼亚寄生虫通过被细胞吸收引起莱什曼尼亚病.
宿主细胞信号通路对于莱什马尼亚感染的建立和持久性至关重要.
了解寄生虫吸收宿主机制是开发新疗法的关键.

研究的目的:

为了研究基因激活蛋白/细胞外信号调节激酶 (MAPK/ERK) 信号传递在巨细胞吸收Leishmania amazonensis中的作用.
为了识别参与莱什马尼亚内部化的宿主细胞激酶.
评估针对莱什曼病中MAPK/ERK信号的治疗潜力.

主要方法:

使用了MAPK/ERK通路组件的小分子抑制剂 (MEK1/2,ERK1/2).
在腺氨酸激酶 (SYK) 和Abl家族激酶中存在遗传缺陷的受雇性巨细胞.
评估了Leishmania amazonensis由巨细胞吸收的前性和前性.
评估了特拉美丁尼布 (一种MEK1/2抑制剂) 在莱什曼病的小鼠模型中的疗效.

主要成果:

ERK1/2信号传递对于莱什曼亚马逊菌被巨细胞吸收至关重要.
抑制MEK1/2或ERK1/2显著降低了Leishmania amastigote内部化的作用.
SYK和Abl家族激酶是Raf,MEK和ERK1/2活动的上游调节者,介导寄生虫吸收.
在感染的小鼠中,特拉美替尼布治疗减少了莱什曼病的严重程度和寄生虫负担,即便是在病变后发病时.

结论:

最大的莱什曼尼亚感染依赖于MAPK/ERK信号通路.
准MAPK/ERK介导的信号传输是莱什曼病的一种有前途的治疗策略.
抑制MEK/ERK信号传递可以减少寄生虫负担和疾病进展.

关键词:

基因酶激酶的使用方法莱什曼尼亚 (Leishmania) 是一种病.在MAPK/ERKK中.巨细胞是一个巨细胞.寄生虫是一种寄生虫.

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