Salmonella biofilms program innate immunity for persistence in Caenorhabditis elegans
Salmonella biofilms program innate immunity for persistence in Caenorhabditis elegans
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DOI：
10.1073/pnas.1822018116
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发表时间：
2019-06-18
影响因子：
11.1
通讯作者：
Kenney, Linda J.
中科院分区：
文献类型：
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作者：
Desai, Stuti K.;Padmanabhan, Anup;Kenney, Linda J.
肠道沙门氏菌生活方式从感染性形式到休眠形式的转换的适应性体内机制仍然未知。我们采用秀丽隐杆线虫作为异源宿主来了解沙门氏菌发病机制的时间动态并确定其体内生活方式。我们发现沙门氏菌在持续感染的C.雅丽根肠在没有体内生物膜的情况下，沙门氏菌通过主动抑制先天免疫途径更快地杀死宿主。两个主要的沙门氏菌致病岛，SPI-1和SPI-2之间的监管串扰，负责生物膜诱导的宿主生理变化，在持续感染。因此，生物膜形成是长期感染中的生存策略，因为延长宿主存活对寄生生活方式有益。
The adaptive in vivo mechanisms underlying the switch in Salmonella enterica lifestyles from the infectious form to a dormant form remain unknown. We employed Caenorhabditis elegans as a heterologous host to understand the temporal dynamics of Salmonella pathogenesis and to identify its lifestyle form in vivo. We discovered that Salmonella exists as sessile aggregates, or in vivo biofilms, in the persistently infected C. elegans gut. In the absence of in vivo biofilms, Salmonella killed the host more rapidly by actively inhibiting innate immune pathways. Regulatory cross-talk between two major Salmonella pathogenicity islands, SPI-1 and SPI-2, was responsible for biofilm-induced changes in host physiology during persistent infection. Thus, biofilm formation is a survival strategy in long-term infections, as prolonging host survival is beneficial for the parasitic lifestyle.