期刊
EMERGING MICROBES & INFECTIONS
卷 10, 期 1, 页码 1849-1861出版社
TAYLOR & FRANCIS LTD
DOI: 10.1080/22221751.2021.1974316
关键词
Salmonella Typhimurium; mouse infection model; systemic infection; SPI-2; comparative proteomics
资金
- National Natural Science Foundation of China [81772149, 82072247]
- Natural Science Foundation of Tianjin [18JCZDJC32400]
- Bacteriology Research Platform of Beijing University of Chinese Medicine
Salmonella enterica serovar Typhimurium triggers reprogramming of host cell metabolism and an inflammatory response during systemic infection, promoting its survival and replication. Additionally, infection by Salmonella may induce M1 and M2 polarization in macrophages, and alter the actin cytoskeleton to facilitate the formation of Salmonella-containing vacuoles.
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.
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