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<p>High-glucose exposure is associated with impaired innate immune function and increased susceptibility to infection; however, its influence on antibiotic–macrophage interactions remains incompletely understood. This study investigated the context-dependent effects of the aminoglycosides streptomycin and kanamycin on murine RAW 264.7 macrophages under low-glucose (5.5&#xa0;mM) and high-glucose (25&#xa0;mM) exposure conditions, used to simulate normoglycemic and hyperglycemic environments. Macrophage viability, phagocytic activity, intracellular bacterial killing, and expression of pro-inflammatory mediators were evaluated following exposure to <i>Escherichia coli</i> ATCC 25922. High-glucose conditions significantly reduced macrophage phagocytosis and intracellular bacterial killing and increased the expression of <i>IL-1β</i>, <i>IL-6</i>, <i>TNF-α</i>, and <i>iNOS</i>. Neither streptomycin nor kanamycin restored phagocytic activity or altered inflammatory gene expression under either glucose condition. In contrast, both aminoglycosides significantly enhanced intracellular bacterial killing under high-glucose exposure, despite persistent impairment of phagocytosis. Cytotoxicity assessments presented concentration-dependent effects of both antibiotics, with macrophage viability preserved at concentrations corresponding to 1× and 2× minimum inhibitory concentration under both glucose conditions. Together, these results indicate that high-glucose exposure is associated with impaired macrophage antimicrobial activity, while aminoglycosides preserve the ability to enhance intracellular bacterial killing under high-glucose exposure without implying direct immunomodulatory effect. This observation underscores the influence of high-glucose environments on antibiotic–host cell interactions.</p>

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Effects of aminoglycosides on macrophage viability and antimicrobial function under high-glucose exposure

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月7日

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  • Piyarat Srinontong,
  • Worapol Aengwanich,
  • Montira Yossapol,
  • Kampeebhorn Boonloh,
  • Zhiliang Wu,
  • Jaroon Wandee

摘要

High-glucose exposure is associated with impaired innate immune function and increased susceptibility to infection; however, its influence on antibiotic–macrophage interactions remains incompletely understood. This study investigated the context-dependent effects of the aminoglycosides streptomycin and kanamycin on murine RAW 264.7 macrophages under low-glucose (5.5 mM) and high-glucose (25 mM) exposure conditions, used to simulate normoglycemic and hyperglycemic environments. Macrophage viability, phagocytic activity, intracellular bacterial killing, and expression of pro-inflammatory mediators were evaluated following exposure to Escherichia coli ATCC 25922. High-glucose conditions significantly reduced macrophage phagocytosis and intracellular bacterial killing and increased the expression of IL-1β, IL-6, TNF-α, and iNOS. Neither streptomycin nor kanamycin restored phagocytic activity or altered inflammatory gene expression under either glucose condition. In contrast, both aminoglycosides significantly enhanced intracellular bacterial killing under high-glucose exposure, despite persistent impairment of phagocytosis. Cytotoxicity assessments presented concentration-dependent effects of both antibiotics, with macrophage viability preserved at concentrations corresponding to 1× and 2× minimum inhibitory concentration under both glucose conditions. Together, these results indicate that high-glucose exposure is associated with impaired macrophage antimicrobial activity, while aminoglycosides preserve the ability to enhance intracellular bacterial killing under high-glucose exposure without implying direct immunomodulatory effect. This observation underscores the influence of high-glucose environments on antibiotic–host cell interactions.