Host metabolic shift during systemic Salmonella infection revealed by comparative proteomics
Salmonella enterica serovar Typhimurium (S. Typhimurium) is a food-borne bacterium that causes acute gastroenteritis in humans and typhoid fever in mice. Salmonella pathogenicity island II (SPI-2) is an important virulence gene cluster responsible for Salmonella survival and replication within host...
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Taylor & Francis Group
2021-01-01
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| Series: | Emerging Microbes and Infections |
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| Online Access: | https://www.tandfonline.com/doi/10.1080/22221751.2021.1974316 |
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| author | Yuanyuan Wang Chunmei Wu Jiacong Gao Xudong Du Xiangyun Chen Mei Zhang |
| author_facet | Yuanyuan Wang Chunmei Wu Jiacong Gao Xudong Du Xiangyun Chen Mei Zhang |
| author_sort | Yuanyuan Wang |
| collection | DOAJ |
| description | Salmonella enterica serovar Typhimurium (S. Typhimurium) is a food-borne bacterium that causes acute gastroenteritis in humans and typhoid fever in mice. Salmonella pathogenicity island II (SPI-2) is an important virulence gene cluster responsible for Salmonella survival and replication within host cells, leading to systemic infection. Previous studies have suggested that SPI-2 function to modulate host vesicle trafficking and immune response to promote systemic infection. However, the molecular mechanism and the host responses triggered by SPI-2 remain largely unknown. To assess the roles of SPI-2, we used a differential proteomic approach to analyse host proteins levels during systemic infections in mice. Our results showed that infection by WT S. Typhimurium triggered the reprogramming of host cell metabolism and inflammatory response. Salmonella systemic infection induces an up-regulation of glycolytic process and a repression of the tricarboxylic acid (TCA) cycle. WT-infected tissues prefer to produce adenosine 5′-triphosphate (ATP) through aerobic glycolysis rather than relying on oxidative phosphorylation to generate energy. Moreover, our data also revealed that infected macrophages may undergo both M1 and M2 polarization. In addition, our results further suggest that SPI-2 is involved in altering actin cytoskeleton to facilitate the Salmonella-containing vacuole (SCV) biogenesis and perhaps even the release of bacteria later in the infection process. Results from our study provide valuable insights into the roles of SPI-2 during systemic Salmonella infection and will guide future studies to dissect the molecular mechanisms of how SPI-2 functions in vivo. |
| format | Article |
| id | doaj-art-c46db9c065fc47fea18d06f77d25e3f6 |
| institution | Kabale University |
| issn | 2222-1751 |
| language | English |
| publishDate | 2021-01-01 |
| publisher | Taylor & Francis Group |
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| series | Emerging Microbes and Infections |
| spelling | doaj-art-c46db9c065fc47fea18d06f77d25e3f62025-08-20T03:49:21ZengTaylor & Francis GroupEmerging Microbes and Infections2222-17512021-01-011011849186110.1080/22221751.2021.1974316Host metabolic shift during systemic Salmonella infection revealed by comparative proteomicsYuanyuan Wang0Chunmei Wu1Jiacong Gao2Xudong Du3Xiangyun Chen4Mei Zhang5TEDA School of Biological Sciences and Biotechnology, Nankai University, Tianjin, People’s Republic of ChinaSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, People’s Republic of ChinaTEDA School of Biological Sciences and Biotechnology, Nankai University, Tianjin, People’s Republic of ChinaTEDA School of Biological Sciences and Biotechnology, Nankai University, Tianjin, People’s Republic of ChinaTEDA School of Biological Sciences and Biotechnology, Nankai University, Tianjin, People’s Republic of ChinaSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, People’s Republic of ChinaSalmonella enterica serovar Typhimurium (S. Typhimurium) is a food-borne bacterium that causes acute gastroenteritis in humans and typhoid fever in mice. Salmonella pathogenicity island II (SPI-2) is an important virulence gene cluster responsible for Salmonella survival and replication within host cells, leading to systemic infection. Previous studies have suggested that SPI-2 function to modulate host vesicle trafficking and immune response to promote systemic infection. However, the molecular mechanism and the host responses triggered by SPI-2 remain largely unknown. To assess the roles of SPI-2, we used a differential proteomic approach to analyse host proteins levels during systemic infections in mice. Our results showed that infection by WT S. Typhimurium triggered the reprogramming of host cell metabolism and inflammatory response. Salmonella systemic infection induces an up-regulation of glycolytic process and a repression of the tricarboxylic acid (TCA) cycle. WT-infected tissues prefer to produce adenosine 5′-triphosphate (ATP) through aerobic glycolysis rather than relying on oxidative phosphorylation to generate energy. Moreover, our data also revealed that infected macrophages may undergo both M1 and M2 polarization. In addition, our results further suggest that SPI-2 is involved in altering actin cytoskeleton to facilitate the Salmonella-containing vacuole (SCV) biogenesis and perhaps even the release of bacteria later in the infection process. Results from our study provide valuable insights into the roles of SPI-2 during systemic Salmonella infection and will guide future studies to dissect the molecular mechanisms of how SPI-2 functions in vivo.https://www.tandfonline.com/doi/10.1080/22221751.2021.1974316Salmonella Typhimuriummouse infection modelsystemic infectionSPI-2comparative proteomics |
| spellingShingle | Yuanyuan Wang Chunmei Wu Jiacong Gao Xudong Du Xiangyun Chen Mei Zhang Host metabolic shift during systemic Salmonella infection revealed by comparative proteomics Emerging Microbes and Infections Salmonella Typhimurium mouse infection model systemic infection SPI-2 comparative proteomics |
| title | Host metabolic shift during systemic Salmonella infection revealed by comparative proteomics |
| title_full | Host metabolic shift during systemic Salmonella infection revealed by comparative proteomics |
| title_fullStr | Host metabolic shift during systemic Salmonella infection revealed by comparative proteomics |
| title_full_unstemmed | Host metabolic shift during systemic Salmonella infection revealed by comparative proteomics |
| title_short | Host metabolic shift during systemic Salmonella infection revealed by comparative proteomics |
| title_sort | host metabolic shift during systemic salmonella infection revealed by comparative proteomics |
| topic | Salmonella Typhimurium mouse infection model systemic infection SPI-2 comparative proteomics |
| url | https://www.tandfonline.com/doi/10.1080/22221751.2021.1974316 |
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