Related Experiment Video
Updated: Sep 26, 2026
Using a Bacterial Pathogen to Probe for Cellular and Organismic-level Host Responses
Published on: February 22, 2019
The response of murine macrophages to infection with Yersinia pestis as revealed by DNA microarray analysis
Lee-Ching Ng1, Ola Forslund, Susie Koh
1Centre for Chemical Defence, DSO National Laboratories, 20 Science Park Drive, Singapore.
Abstract:
Macrophages play a crucial role in recognition and phagocytosis of pathogens and in the induction of response, immunity and immunopathology. A key strategy employed by numerous pathogens such as Yersinia pestis is to circumvent the immune response of the host via actively down-regulating the activation of macrophages. The study on host-pathogen interaction and gene expression is imperative for the development of alternative therapeutics. We have combined Suppression Subtractive Hybridisation (SSH), Microarray techniques, Northern blot analysis and quantitative reverse transcription coupled PCR (RT-PCR) to gain a view of differential host gene expression in response to Y. pestis-26 degrees C infection. In our study, a total of 22 different genes were identified as up-regulated in response to the Y. pestis infection. These genes include unknown EST's, cytokines, enzyme of cytokine, receptors, ligands, transcriptional factors, inhibitor of transcriptional factor, and proteins involved with cytoskeleton. More interestingly, among them are 7 genes that encode for factors known to be associated with cell cycling and cell proliferation, with 3 of them playing a role in apoptosis. Our data also indicate that macrophage cells undergo apoptosis during an infection with Y. pestis-37 degrees C, however an infection with 26 degrees C cultures results in a delayed apoptosis. The correlation between the delayed apoptosis and the up-regulation of anti-apoptotic gene is currently being studied.
Insights
Yersinia pestis infection alters macrophage gene expression, up-regulating 22 genes, including those involved in cell cycling and apoptosis. This Y. pestis study reveals delayed apoptosis at 26°C, impacting host-pathogen interactions.
Area of Science:
- Immunology
- Microbiology
- Molecular Biology
Background:
- Macrophages are key immune cells involved in pathogen recognition and host response.
- Pathogens like Yersinia pestis can evade immune responses by down-regulating macrophage activation.
- Understanding host-pathogen interactions at the gene expression level is vital for developing new therapeutics.
Purpose of the Study:
- To investigate differential host gene expression in macrophages during Yersinia pestis infection.
- To identify specific genes modulated by Y. pestis infection at different temperatures (26°C vs. 37°C).
Main Methods:
- Suppression Subtractive Hybridisation (SSH)
- Microarray analysis
- Northern blot analysis
- Quantitative reverse transcription coupled PCR (RT-PCR)
Main Results:
- Identified 22 up-regulated genes in response to Y. pestis infection.
- These genes include those related to cytokines, receptors, transcriptional factors, and cytoskeleton.
- Observed delayed apoptosis in macrophages infected with Y. pestis at 26°C compared to 37°C.
- Found 7 genes associated with cell cycling and proliferation, including 3 involved in apoptosis.
Conclusions:
- Yersinia pestis infection significantly impacts macrophage gene expression.
- The temperature-dependent modulation of apoptosis suggests a potential immune evasion strategy by Y. pestis.
- Further research is ongoing to explore the link between up-regulated anti-apoptotic genes and delayed apoptosis.
