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Purpose <p>Natural killer (NK) cells contribute to tumour immunosurveillance. They detect and eliminate circulating tumour cells by degranulation, releasing perforin and granzyme. Also involved in NK-cell-mediated tumour cell defense are cytokines with proapoptotic and anti-apoptotic characteristics as well as extracellular vesicles containing perforin. Recent clinical studies suggest that volatile anesthetics might negatively impact cancer outcomes compared with intravenous agents. A possible factor could be the impairment of NK cell activity by volatile anesthetics. In this study, we aimed to investigate the effects of sevoflurane on NK-mediated tumour cell defense in a cell model <i>in vitro</i>.</p> Methods <p>In an <i>in vitro</i> laboratory study, we exposed a NK cell line to 2.2% sevoflurane for 2 hr, followed by co-incubation with leukemia target cells. We defined apoptosis of targeted tumour cells and explored effector cell mechanisms by assessing degranulation of NK92 cells and production of cytokine messenger ribonucleic acid (mRNA). Furthermore, we determined NK cell concentrations of extracellular vesicles and perforin protein.</p> Results <p>After 24 hr of co-incubation of tumour cells with sevoflurane-pretreated NK cells, the number of early apoptotic tumour cells was decreased, with a reduction of 36% on average (<i>P</i> = 0.016). Natural killer cell degranulation, cytokine mRNA, and size and concentration of extracellular vesicles were not significantly different. The perforin concentration of NK cells was reduced when pretreated with sevoflurane. At 48 hr, perforin cell content as well as perforin in the supernatant was reduced (mean reduction for both, 16%; <i>P</i> &lt; 0.001 for both).</p> Conclusions <p>This study suggests that the observed transient impaired NK-cell-mediated tumour defense may be linked to the reduced perforin production when NK cells are exposed to sevoflurane.</p>

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Effects of sevoflurane on natural killer cell-induced apoptosis of malignant tumour cells: an in vitro laboratory study

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月27日

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  • Valérie Rössler-Fehr,
  • Jonah B. Neff,
  • Suellen Darc dos Santos Oliveira,
  • Zhenlong Chen,
  • Richard D. Minshall,
  • Martin Schläpfer,
  • Beatrice Beck-Schimmer

摘要

Purpose

Natural killer (NK) cells contribute to tumour immunosurveillance. They detect and eliminate circulating tumour cells by degranulation, releasing perforin and granzyme. Also involved in NK-cell-mediated tumour cell defense are cytokines with proapoptotic and anti-apoptotic characteristics as well as extracellular vesicles containing perforin. Recent clinical studies suggest that volatile anesthetics might negatively impact cancer outcomes compared with intravenous agents. A possible factor could be the impairment of NK cell activity by volatile anesthetics. In this study, we aimed to investigate the effects of sevoflurane on NK-mediated tumour cell defense in a cell model in vitro.

Methods

In an in vitro laboratory study, we exposed a NK cell line to 2.2% sevoflurane for 2 hr, followed by co-incubation with leukemia target cells. We defined apoptosis of targeted tumour cells and explored effector cell mechanisms by assessing degranulation of NK92 cells and production of cytokine messenger ribonucleic acid (mRNA). Furthermore, we determined NK cell concentrations of extracellular vesicles and perforin protein.

Results

After 24 hr of co-incubation of tumour cells with sevoflurane-pretreated NK cells, the number of early apoptotic tumour cells was decreased, with a reduction of 36% on average (P = 0.016). Natural killer cell degranulation, cytokine mRNA, and size and concentration of extracellular vesicles were not significantly different. The perforin concentration of NK cells was reduced when pretreated with sevoflurane. At 48 hr, perforin cell content as well as perforin in the supernatant was reduced (mean reduction for both, 16%; P < 0.001 for both).

Conclusions

This study suggests that the observed transient impaired NK-cell-mediated tumour defense may be linked to the reduced perforin production when NK cells are exposed to sevoflurane.