Proinflammatory cytokine mRNA responses in experimental Burkholderia pseudomallei infection in mice
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Updated: Oct 17, 2026
A Non-invasive and Technically Non-intensive Method for Induction and Phenotyping of Experimental Bacterial Pneumonia in Mice
Published on: September 28, 2016
G C Ulett1, N Ketheesan, R G Hirst
1Department of Microbiology and Immunology, James Cook University, Townsville, Queensland, Australia. glen.ulett@jcu.edu.au
Abstract:
Melioidosis is a potentially fatal disease of both human and animals caused by the bacterium Burkholderia pseudomallei. Disease is endemic in tropical and subtropical regions of Southeast Asia and Northern Australia. The pathogenesis of melioidosis is poorly understood. In particular, the host responses that occur following infection, and the specific host-pathogen interactions that result in the development of either acute or chronic infection are unclear. Using an established murine model, we investigated early proinflammatory cytokine responses believed to be critical in the development of acute and chronic B. pseudomallei infection. Semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) was used to assess levels of mRNA for tumor necrosis factor-alpha (TNF-alpha), interleukin 1beta (IL-1beta) and interleukin 6 (IL-6) in the liver of mice following infection. We demonstrate that the level of mRNA for these cytokines increase moderately in chronic infection in C57BL/6 mice. However, in acute infection in BALB/c mice, mRNA responses for these cytokines were shown to be comparatively greater. These results demonstrate that early proinflammatory cytokine responses are important in the immunopathogenesis of melioidosis.
Insights
This study reveals that early inflammatory responses, specifically tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6, are crucial in melioidosis pathogenesis. Acute infections in BALB/c mice showed greater cytokine mRNA levels compared to chronic infections in C57BL/6 mice.
Area of Science:
- Immunology
- Microbiology
- Pathogenesis
Background:
- Melioidosis, caused by Burkholderia pseudomallei, is a severe disease endemic in tropical regions.
- The precise mechanisms of host response and host-pathogen interactions leading to acute or chronic melioidosis remain unclear.
- Early proinflammatory cytokine responses are hypothesized to play a critical role in disease development.
Purpose of the Study:
- To investigate early proinflammatory cytokine responses in a murine model of B. pseudomallei infection.
- To correlate cytokine mRNA levels with the development of acute versus chronic melioidosis.
- To elucidate the role of specific cytokines in the immunopathogenesis of melioidosis.
Main Methods:
- Utilized a murine model of B. pseudomallei infection.
- Employed semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) to measure mRNA levels.
- Assessed mRNA expression for tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and interleukin-6 (IL-6) in liver tissue.
Main Results:
- Demonstrated a moderate increase in cytokine mRNA levels in chronic infections (C57BL/6 mice).
- Observed comparatively greater mRNA responses for these cytokines during acute infections (BALB/c mice).
- Highlighted differential cytokine expression patterns between acute and chronic infection models.
Conclusions:
- Early proinflammatory cytokine responses are integral to the immunopathogenesis of melioidosis.
- The magnitude of cytokine response may differentiate between acute and chronic disease outcomes.
- Findings contribute to understanding host-pathogen dynamics in B. pseudomallei infections.
