earticle

영어

Antibiotic-resistant bacteria have increasingly emerged as a significant global health challenge in the effective treatment of bacterial infections. Therefore, we conducted this study to evaluate the antibacterial efficacy of nitric oxide (NO) water and its influence on RAW 264.7 macrophage immune cell line during bacterial infections. The experiment was divided into four groups: NC (normal control), NT (cells + NO water), infected group (each bacterial strains), and treatment group (infected + NO water). NO water was generated using device by bubbling NO gas into tap water, thereby generating final concentrations of 100, 175, and 250 μM. The antibacterial activity was assessed against five different pathogenic bacterial strains such as Escherichia coli (E. coli), Salmonella pullorum (S. pullorum), Staphylococcus aureus (S. aureus), Pseudomonas aeruginosa (P. aeruginosa), and Helicobacter pylori (H. pylori). Colony-forming unit (CFU) assays revealed a significant reduction in bacterial growth, with 250 μM NO water exhibiting the strongest antimicrobial effects. In particular, E. coli and S. aureus were the most susceptible, showing over a 90% reduction in CFU counts as compared to the control group. Moreover, P. aeruginosa, S. pullorum, and H. pylori also significantly decreased bacterial counts as compared to the control group. Furthermore, the effects of NO water on immune cell activation was assessed by treating RAW264.7 macrophages cell line to bacterial infection and measuring post-treatment cell viability, reactive oxygen species (ROS), and NO production. At 30 μM NO water, a significant increase in cell viability was observed 6 hours post-infection, particularly in S. aureus and S. pullorum-infected macrophages. However, cell viability decreased at 12 and 24 hours, indicating a time-dependent response. NO water significantly reduced ROS levels in E. coli, P. aeruginosa, and H. pylori-infected cells, thereby mitigating oxidative stress. In contrast, S. aureusinfected cells, ROS levels were increased, suggesting a pathogen-specific response. Additionally, NO water significantly increased intracellular NO levels in bacteria-infected RAW264.7 cells, particularly in infections with S. aureus, E. coli, and S. pullorum. Collectively, our findings suggest that NO water enhances NO synthesis, decreases ROS production, modulates immune responses, and facilitates pathogen clearance. However, further more in-depth in vivo and clinical studies are necessary to fully elucidate its underlying mechanisms.