Related Experiment Video
Updated: May 23, 2026

High-throughput Assay to Phenotype Salmonella enterica Typhimurium Association, Invasion, and Replication in Macrophages
Published on: August 11, 2014
Acidic pH induced STM1485 gene is essential for intracellular replication of Salmonella
Uday Sankar Allam1, M Gopala Krishna, Minakshi Sen
1Department of Microbiology, Centre for Infectious Disease Research and Biosafety Laboratories, Indian Institute of Science, Bangalore, India.
Abstract:
During the course of infection, Salmonella has to face several potentially lethal environmental conditions, one such being acidic pH. The ability to sense and respond to the acidic pH is crucial for the survival and replication of Salmonella. The physiological role of one gene (STM1485) involved in this response, which is upregulated inside the host cells (by 90- to 113-fold) is functionally characterized in Salmonella pathogenesis. In vitro, the ΔSTM1485 neither exhibited any growth defect at pH 4.5 nor any difference in the acid tolerance response. The ΔSTM1485 was compromised in its capacity to proliferate inside the host cells and complementation with STM1485 gene restored its virulence. We further demonstrate that the surface translocation of Salmonella pathogenicity island-2 (SPI-2) encoded translocon proteins, SseB and SseD were reduced in the ΔSTM1485. The increase in co-localization of this mutant with lysosomes was also observed. In addition, the ΔSTM1485 displayed significantly reduced competitive indices (CI) in spleen, liver and mesenteric lymph nodes in murine typhoid model when infected by intra-gastric route. Based on these results, we conclude that the acidic pH induced STM1485 gene is essential for intracellular replication of Salmonella.
Insights
The Salmonella gene STM1485, induced by acidic pH, is vital for bacterial survival within host cells. Its absence impairs Salmonella
Area of Science:
- Microbiology
- Bacterial Pathogenesis
- Infectious Diseases
Background:
- Salmonella infection survival depends on adapting to host environmental challenges, including acidic pH.
- Acidic conditions are encountered by Salmonella during host cell invasion and intracellular replication.
- Gene STM1485 is significantly upregulated by Salmonella within host cells, suggesting a role in pathogenesis.
Purpose of the Study:
- To functionally characterize the role of the acid-induced gene STM1485 in Salmonella pathogenesis.
- To investigate the impact of STM1485 on Salmonella survival, replication, and virulence within host cells and in vivo.
Main Methods:
- Construction and in vitro analysis of a ΔSTM1485 mutant for growth and acid tolerance.
- Assessment of intracellular replication and virulence of the mutant within host cells.
- Evaluation of Salmonella pathogenicity island-2 (SPI-2) translocon protein translocation (SseB, SseD).
- Murine typhoid model infection via intra-gastric route to determine competitive indices (CI) in spleen, liver, and lymph nodes.
Main Results:
- The ΔSTM1485 mutant showed no growth defect at acidic pH (4.5) or altered acid tolerance response in vitro.
- Intracellular proliferation of the ΔSTM1485 mutant within host cells was significantly compromised, with virulence restored upon complementation.
- Surface translocation of SPI-2 translocon proteins SseB and SseD was reduced in the mutant, correlating with increased co-localization with lysosomes.
- The ΔSTM1485 mutant exhibited significantly reduced competitive indices in murine spleen, liver, and mesenteric lymph nodes.
Conclusions:
- The acidic pH-induced gene STM1485 is essential for intracellular replication of Salmonella.
- STM1485 plays a critical role in Salmonella pathogenesis by facilitating intracellular survival and proliferation, likely through modulation of SPI-2 function.
- Targeting STM1485 may represent a novel strategy to combat Salmonella infections.
Related Concept Videos
DNA Bacteriophages
Stringent Response in E. coli
Bacterial Gastroenteritis
Lysogenic Cycle of Bacteriophages
Gene Regulation During Sporulation
Viral Replication: Lysogenic Cycle

