Depletion of reactive oxygen species induced by chlorogenic acid triggers apoptosis-like death in Escherichia coli

Abstract

Chlorogenic acid (CGA) is a phenolic compound with various health-promoting properties, including antioxidant effects and a wide range of antibacterial activities. However, the antibacterial mechanism remains unclear. We investigated the underlying mode of action of CGA against Escherichia coli, which shows bacterial apoptosis-like death. Cells treated with CGA showed apoptotic features such as membrane depolarisation, caspase-like protein expression, increased intracellular Ca²⁺ levels, phosphatidylserine externalisation, and DNA fragmentation. In contrast to common bacterial apoptosis-like death, which is caused by reactive oxygen species (ROS) accumulation, CGA depleted intracellular ROS. Because ROS are important intracellular signalling molecules, and ROS depletion may affect bacterial intracellular signalling pathways, leading to cell death. To determine whether deficiencies in intracellular ROS cause apoptosis-like death, the cells were treated with H₂O₂ after CGA treatment. H₂O₂ restored depleted intracellular ROS levels to similar levels as in untreated cells, and cell viability was increased compared to CGA-treated cells. Moreover, apoptotic features were attenuated in H₂O₂ post-treated cells. These results demonstrate that CGA induces bacterial apoptosis in E. coli and intracellular ROS depletion is a core regulator in the progression of bacterial apoptosis-like death.

Keywords:

• Antibacterial mechanism
• bacterial apoptosis-like death
• chlorogenic acid
• Escherichia coli
• reactive oxygen species depletion

Disclosure statement

The authors declare that there are no conflicts of interest.

Additional information

Funding

This research was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT and Future Planning [2017R1A2B4005811].