Tsaplina Olga, Artamonova Tatiana, Khodorkovsky Mikhail, Khmel Inessa
Institute of Cytology, Russian Academy of Sciences, Tikhoretsky av. 4, St Petersburg, Russia, 194064.
Department of Nanobiotechnologies, Peter the Great St. Petersburg Polytechnic University, St. Petersburg, Russia, 195251.
Arch Microbiol. 2025 Sep 18;207(11):266. doi: 10.1007/s00203-025-04475-0.
The rhizobacteria Serratia plymuthica are considered promising antimicrobial agents. However, cases of infection of both plants and humans by these bacteria have been described. espite the various mechanisms of infection of plants and humans, cases cross-kingdom pathogenicity of bacteria are increasingly being recorded. The aim of the work was to assess the possibility of infection of human cells by S. plymuthica. Using confocal microscopy and a quantitative microbiological method, we showed for the first time that S. plymuthica IC1270 is able to penetrate M-HeLa cells. And the Quorum Sensing system and the global gene regulation system GrrA/GrrS determine the intensity of their invasion. Surprisingly, inactivation of the grrA gene reduces invasion, in contrast to inactivation of the grrS gene, which increases invasion. For penetration, these bacteria use the host cell α5β1 integrin, the intensity of expression of which increases as a result of infection. Moreover, the intensity of invasion upon gene inactivation correlate with the intensity of expression of α5 and β1 integrin subunits. The increased expression of these genes is due to contact with the Serratia surface protein OmpX, which is regulated by GrrA and GrrS. An additional factor that enhances invasion upon inactivation of the grrS gene may be the accumulation of isomerase PpiA, which mediates the folding of surface proteins. Thus, S. plymuthica penetrates M-HeLa cells using α5β1 integrin, the expression of which is regulated by the GrrA/GrrS-dependent surface protein of bacteria.
根际细菌普城沙雷氏菌被认为是很有前景的抗菌剂。然而，已经有这些细菌感染植物和人类的病例报道。尽管植物和人类的感染机制各不相同，但细菌跨界致病性的病例记录越来越多。这项工作的目的是评估普城沙雷氏菌感染人类细胞的可能性。利用共聚焦显微镜和定量微生物学方法，我们首次表明普城沙雷氏菌IC1270能够穿透M-HeLa细胞。群体感应系统和全局基因调控系统GrrA/GrrS决定了它们的入侵强度。令人惊讶的是，与增加入侵的grrS基因失活相反，grrA基因失活会降低入侵。为了实现穿透，这些细菌利用宿主细胞α5β1整合素，其表达强度因感染而增加。此外，基因失活后的入侵强度与α5和β1整合素亚基的表达强度相关。这些基因表达的增加是由于与受GrrA和GrrS调控的沙雷氏菌表面蛋白OmpX接触所致。grrS基因失活后增强入侵的另一个因素可能是异构酶PpiA的积累，它介导表面蛋白的折叠。因此，普城沙雷氏菌利用α5β1整合素穿透M-HeLa细胞，其表达受细菌GrrA/GrrS依赖性表面蛋白调控。
