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Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
Published on: May 21, 2018
An avian pathogenic Escherichia coli isolate induces caspase 3/7 activation in J774 macrophages
Michele Bastiani1, Marilda Carlos Vidotto, Fabiana Horn
1Departamento de Biofísica, Universidade Federal do Rio Grande do Sul, P.O. Box 15005, 91501-970 Porto Alegre, RS, Brazil.
Abstract:
Avian pathogenic Escherichia coli (APEC) strains, the etiological agent of colibacillosis in poultry, must resist the attack of incoming macrophages in order to cause disease. In this work, we show that an APEC strain (APEC17) remained viable inside J774 macrophages for at least 8 h and was cytotoxic to them 6-8 h after infection. APEC17 induced caspase 3/7 activation, the central caspases in apoptosis, in infected macrophages already at 2h after infection. Both cytotoxicity and caspase 3/7 activation were reduced when cells were infected with heat-killed APEC17, showing that bacteria must be viable to induce apoptosis. Our findings using APEC17 suggest that APEC may escape destruction by triggering macrophage apoptotic death.
Insights
Avian pathogenic Escherichia coli (APEC) triggers apoptosis in host macrophages, allowing the bacteria to survive and cause disease. Viable APEC strains induce macrophage death, crucial for colibacillosis development in poultry.
Area of Science:
- Veterinary Microbiology
- Immunology
- Cell Biology
Background:
- Avian pathogenic Escherichia coli (APEC) causes colibacillosis in poultry.
- APEC must evade host immune responses, particularly macrophages, to establish infection.
Purpose of the Study:
- To investigate the interaction between APEC and macrophages.
- To determine if APEC induces macrophage apoptosis and if bacterial viability is required.
Main Methods:
- Infection of J774 macrophages with viable and heat-killed APEC17.
- Assessment of bacterial viability within macrophages over time.
- Measurement of macrophage cytotoxicity and caspase 3/7 activation.
Main Results:
- APEC17 survived within macrophages for at least 8 hours.
- APEC17 induced macrophage cytotoxicity and caspase 3/7 activation starting at 2 hours post-infection.
- Both cytotoxicity and apoptosis induction were significantly reduced with heat-killed APEC17.
Conclusions:
- Viable APEC actively induces apoptosis in macrophages.
- This mechanism allows APEC to escape immune destruction and contributes to disease pathogenesis.
- APEC employs apoptotic cell death as a survival strategy against host defenses.
