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Updated: May 8, 2026

Isolation of Salmonella typhimurium-containing Phagosomes from Macrophages
Published on: October 25, 2017
Responses of macrophages against Salmonella infection compared with phagocytosis
Maozhi Hu1, Yun Yang, Chuang Meng
1Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou University, Yangzhou, 225009, People's Republic of China.
Abstract:
To explore the responses of host cell after infection with live Salmonella compared with phagocytosis to dead bacteria, the responses of mouse macrophage after infection with Salmonella enteritidis C50041 and the fixed C50041 (C50041-d) were analyzed. Results indicated that the cytotoxicity induced by C50041 was stronger than C50041-d. Similar changing trends of mitochondrial membrane potential, intracellular concentration of calcium ions, reactive oxygen species and nitric oxide were found between C50041 and C50041-d infection. But the cell responses against C50041 were earlier and stronger than C50041-d. LC3 expression of macrophage induced by C50041 was lower than C50041-d. C50041 significantly inhibited the production of tumor necrosis factor and interleukin (IL)-6. Whereas intracellular caspase-1 activation and IL-1β release induced by C50041 were stronger than C50041-d, caspase-1 activation and IL-1β release are the innate defense responses of macrophage. Therefore, it will be beneficial to explore the use of this pathway in the control of Salmonella infection.
Insights
Live Salmonella enteritidis triggered earlier and stronger host cell responses, including caspase-1 activation and IL-1β release, compared to dead bacteria. This suggests targeting these innate defense pathways could control Salmonella infection.
Area of Science:
- Immunology
- Microbiology
Background:
- Host-pathogen interactions are crucial for understanding infection dynamics.
- Salmonella enteritidis infection elicits complex macrophage responses.
Purpose of the Study:
- To compare host macrophage responses to live versus dead Salmonella enteritidis.
- To identify key cellular pathways involved in Salmonella infection.
Main Methods:
- Infection of mouse macrophages with live Salmonella enteritidis C50041 and fixed C50041 (C50041-d).
- Analysis of cytotoxicity, mitochondrial membrane potential, intracellular calcium ions, reactive oxygen species, nitric oxide, LC3 expression, tumor necrosis factor, IL-6, caspase-1 activation, and IL-1β release.
Main Results:
- Live Salmonella induced stronger cytotoxicity and earlier, more robust cellular responses than dead bacteria.
- While trends in mitochondrial potential and ion concentrations were similar, live Salmonella led to lower LC3 expression.
- Live Salmonella significantly inhibited TNF and IL-6 but enhanced caspase-1 activation and IL-1β release.
Conclusions:
- Host macrophage responses are significantly different between live and dead Salmonella enteritidis.
- Enhanced caspase-1 activation and IL-1β release by live Salmonella indicate crucial innate defense mechanisms.
- Targeting the caspase-1/IL-1β pathway presents a potential strategy for controlling Salmonella infections.
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