感染了……的GSPD-1缺陷型小鼠的免疫反应和屏障功能受损。 （注：原文中“infected with.”后面缺少具体病原体信息）
Impaired immune response and barrier function in GSPD-1-deficient infected with .
作者信息
Yang Wan-Hua, Chen Po-Hsiang, Chang Hung-Hsin, Kwok Hong Luen, Stern Arnold, Soo Po-Chi, Chen Jiun-Han, Yang Hung-Chi
机构信息
Department of Pathology and Laboratory Medicine, Taipei Veterans General Hospital, Hsinchu Branch, Hsinchu, Taiwan.
Research Center for Chinese Herbal Medicine, Graduate Institute of Health Industry Technology, College of Human Ecology, Chang Gung University of Science and Technology, Taoyuan, Taiwan.
出版信息
Curr Res Microb Sci. 2023 Jan 27;4:100181. doi: 10.1016/j.crmicr.2023.100181. eCollection 2023.
-RNAi knockdown was used as an immune-compromised model to investigate the role of G6PD in host-pathogen interactions. A shorted lifespan, increased bacterial burden and bacterial translocation were observed in -knockdown infected with (KP). RNAseq revealed that the innate immune pathway, including and , was affected by knockdown. qPCR confirmed that tight junction ) and immune-associated genes () were down-regulated in -knockdown and following infection with KP. The down-regulation of antimicrobial effector lysozymes, including and , was found in -knockdown infected with KP. Deletion of , and in -knockdown infected with KP abolished the shorten lifespan seen in the Mock control. GSPD-1 deficiency in resulted in bacterial accumulation and lethality, possibly due to a defective immune response. These findings indicate that GSPD-1 has a protective role in microbial defense in by preventing bacterial colonization through bacterial clearance.
RNA干扰敲低被用作免疫受损模型，以研究葡萄糖-6-磷酸脱氢酶（G6PD）在宿主-病原体相互作用中的作用。在感染肺炎克雷伯菌（KP）的敲低模型中观察到寿命缩短、细菌负荷增加和细菌易位。RNA测序显示，包括Toll样受体和NOD样受体在内的固有免疫途径受到敲低的影响。定量聚合酶链反应（qPCR）证实，在敲低模型以及感染KP后，紧密连接和免疫相关基因被下调。在感染KP的敲低模型中发现，包括溶菌酶和溶菌酶在内的抗菌效应物溶菌酶被下调。在感染KP的敲低模型中删除特定基因可消除在模拟对照中看到的寿命缩短现象。秀丽隐杆线虫中GSPD-1的缺乏导致细菌积累和致死率，这可能是由于免疫反应缺陷所致。这些发现表明，GSPD-1通过清除细菌来防止细菌定植，从而在秀丽隐杆线虫的微生物防御中发挥保护作用。
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