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Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
Published on: May 21, 2018
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Inflammasome activation by Campylobacter jejuni
Lieneke I Bouwman1, Marcel R de Zoete2, Nancy M C Bleumink-Pluym1
1Department of Infectious Diseases and Immunology, Utrecht University, 3584 CL Utrecht, the Netherlands;
Journal of Immunology (Baltimore, Md. : 1950)
|October 1, 2014
Summary
Campylobacter jejuni infection activates the NLRP3 inflammasome in macrophages, leading to IL-1β secretion without cell death. This bacterial foodborne pathogen
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Campylobacter jejuni is a leading cause of bacterial foodborne illness globally.
- Mechanisms of C. jejuni invasion and intestinal inflammation remain unclear.
Purpose of the Study:
- To investigate the role of the NLRP3 inflammasome in C. jejuni infection.
- To understand C. jejuni-induced immune responses in macrophages.
Main Methods:
- Infection of mouse and human macrophages with C. jejuni.
- Analysis of inflammasome components (NLRP3, ASC, caspase-1/11) and IL-1β secretion.
- Utilized various C. jejuni mutants to assess invasion and inflammasome activation.
Main Results:
- C. jejuni induced pro-IL-1β transcription and IL-1β secretion in macrophages without cell death.
- NLRP3, ASC, and caspase-1/11 were essential for C. jejuni-induced IL-1β secretion.
- Activation occurred independently of priming and correlated with intracellular bacterial numbers.
Conclusions:
- C. jejuni activates the NLRP3 inflammasome in a non-cytotoxic manner, even in non-primed cells.
- This pathway contributes to C. jejuni-induced intestinal inflammation.
- Expands the understanding of bacterial inflammasome activation mechanisms.
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