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Outer Membrane Vesiculation Facilitates Surface Exchange and In Vivo Adaptation of Vibrio cholerae.
Cell Host & Microbe ( IF 20.6 ) Pub Date : 2019-12-31 , DOI: 10.1016/j.chom.2019.12.002 Franz G Zingl 1 , Paul Kohl 1 , Fatih Cakar 1 , Deborah R Leitner 1 , Fabian Mitterer 1 , Katherine E Bonnington 2 , Gerald N Rechberger 3 , Meta J Kuehn 2 , Ziqiang Guan 4 , Joachim Reidl 5 , Stefan Schild 5
Cell Host & Microbe ( IF 20.6 ) Pub Date : 2019-12-31 , DOI: 10.1016/j.chom.2019.12.002 Franz G Zingl 1 , Paul Kohl 1 , Fatih Cakar 1 , Deborah R Leitner 1 , Fabian Mitterer 1 , Katherine E Bonnington 2 , Gerald N Rechberger 3 , Meta J Kuehn 2 , Ziqiang Guan 4 , Joachim Reidl 5 , Stefan Schild 5
Affiliation
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Gram-negative bacteria release outer membrane vesicles into the external milieu to deliver effector molecules that alter the host and facilitate virulence. Vesicle formation is driven by phospholipid accumulation in the outer membrane and regulated by the phospholipid transporter VacJ/Yrb. We use the facultative human pathogen Vibrio cholerae to show that VacJ/Yrb is silenced early during mammalian infection, which stimulates vesiculation that expedites bacterial surface exchange and adaptation to the host environment. Hypervesiculating strains rapidly alter their bacterial membrane composition and exhibit enhanced intestinal colonization fitness. This adaptation is exemplified by faster accumulation of glycine-modified lipopolysaccharide (LPS) and depletion of outer membrane porin OmpT, which confers resistance to host-derived antimicrobial peptides and bile, respectively. The competitive advantage of hypervesiculation is lost upon pre-adaptation to bile and antimicrobial peptides, indicating the importance of these adaptive processes. Thus, bacteria use outer membrane vesiculation to exchange cell surface components, thereby increasing survival during mammalian infection.
中文翻译：
外膜囊泡促进霍乱弧菌的表面交换和体内适应。
革兰氏阴性细菌将外膜囊泡释放到外部环境中以传递效应分子，从而改变宿主并促进毒力。囊泡的形成是由外膜中的磷脂积累驱动的，并受磷脂转运蛋白 VacJ/Yrb 的调节。我们使用兼性人类病原体霍乱弧菌来表明 VacJ/Yrb 在哺乳动物感染期间早期被沉默，这会刺激水泡形成，从而加速细菌表面交换和对宿主环境的适应。高泡菌株迅速改变其细菌膜组成并表现出增强的肠道定植适应性。这种适应表现为甘氨酸修饰脂多糖 (LPS) 的更快积累和外膜孔蛋白 OmpT 的消耗，分别赋予宿主来源的抗微生物肽和胆汁抗性。在预先适应胆汁和抗菌肽后，过度膀胱的竞争优势就会消失，这表明这些适应过程的重要性。因此，细菌使用外膜囊泡交换细胞表面成分，从而提高哺乳动物感染期间的存活率。
更新日期：2019-12-31
中文翻译：
外膜囊泡促进霍乱弧菌的表面交换和体内适应。
革兰氏阴性细菌将外膜囊泡释放到外部环境中以传递效应分子，从而改变宿主并促进毒力。囊泡的形成是由外膜中的磷脂积累驱动的，并受磷脂转运蛋白 VacJ/Yrb 的调节。我们使用兼性人类病原体霍乱弧菌来表明 VacJ/Yrb 在哺乳动物感染期间早期被沉默，这会刺激水泡形成，从而加速细菌表面交换和对宿主环境的适应。高泡菌株迅速改变其细菌膜组成并表现出增强的肠道定植适应性。这种适应表现为甘氨酸修饰脂多糖 (LPS) 的更快积累和外膜孔蛋白 OmpT 的消耗，分别赋予宿主来源的抗微生物肽和胆汁抗性。在预先适应胆汁和抗菌肽后，过度膀胱的竞争优势就会消失，这表明这些适应过程的重要性。因此，细菌使用外膜囊泡交换细胞表面成分，从而提高哺乳动物感染期间的存活率。
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