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Amygdalin Reverses Macrophage PANoptosis Induced by Drug-Resistant Escherichia coli
Xue Yan1, Liang Jin1, Huifen Zhou2
1School of Life Sciences, Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310053, P.R. China.
Abstract:
Infectious diseases caused by drug-resistant Escherichia coli (E. coli) pose a critical concern for medical institutions as they can lead to high morbidity and mortality rates. In this study, amygdalin exhibited anti-inflammatory and antioxidant activities, as well as other potentials. However, whether it could influence the drug-resistant E. coli-infected cells remained unanswered. Amygdalin was therefore tested in a cellular model in which human macrophages were exposed to resistant E. coli. Apoptosis was measured by flow cytometry and the lactate dehydrogenase (LDH) assay. Western immunoblotting and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) were used to quantify interleukin-18 (IL-18), interleukin-1β (IL-1β), and interleukin-6 (IL-6). The production of reactive oxygen species (ROS) in macrophages was detected by ROS kit. The expression of panapoptotic proteins in macrophages was measured by qRT-PCR and Western immunoblotting. Drug-Resistant E. coli inhibited cell viability and enhanced apoptosis in the cellular model. In cells treated with amygdalin, this compound can inhibit cell apoptosis and reduce the expression of pro - inflammatory cytokines such as IL-1β, IL-18 and IL-6. Additionally, it decreases the production of PANoptosis proteins, Furthermore, amygdalin lowered the levels of reactive oxygen species induced by drug-resistant E. coli, in cells, demonstrating its antioxidant effects. Amygdalin, a drug with a protective role, alleviated cell damage caused by drug-resistant E. coli in human macrophages by inhibiting the PANoptosis signaling pathway.
Insights
Amygdalin protects human macrophages from drug-resistant Escherichia coli (E. coli) by reducing inflammation and cell death. This study shows amygdalin
Area of Science:
- Immunology
- Pharmacology
- Microbiology
Background:
- Drug-resistant Escherichia coli (E. coli) infections present a significant health risk, leading to severe illness and fatalities.
- Amygdalin is known for its anti-inflammatory and antioxidant properties, but its effects on drug-resistant E. coli-infected cells were unclear.
Purpose of the Study:
- To investigate the protective effects of amygdalin against drug-resistant E. coli-induced damage in human macrophages.
- To elucidate the mechanisms by which amygdalin modulates inflammatory responses and cell death pathways.
Main Methods:
- Human macrophages were exposed to drug-resistant E. coli, with or without amygdalin treatment.
- Apoptosis, cytokine levels (IL-1β, IL-18, IL-6), reactive oxygen species (ROS), and panoptosis-related proteins were quantified.
- Techniques included flow cytometry, LDH assay, Western immunoblotting, and quantitative reverse-transcription polymerase chain reaction (qRT-PCR).
Main Results:
- Drug-resistant E. coli reduced cell viability and increased apoptosis and pro-inflammatory cytokine production.
- Amygdalin treatment inhibited E. coli-induced apoptosis, decreased levels of IL-1β, IL-18, and IL-6, and reduced ROS production.
- Amygdalin also decreased the expression of panoptosis proteins, indicating inhibition of the PANoptosis signaling pathway.
Conclusions:
- Amygdalin demonstrates a protective role against drug-resistant E. coli in human macrophages.
- It alleviates cell damage by inhibiting the PANoptosis signaling pathway, reducing inflammation, and mitigating oxidative stress.
