Scholarlink

<p><i>Staphylococcus aureus</i> is a major pathogen responsible for a wide range of infections, from minor skin diseases to life-threatening conditions, such as sepsis and pneumonia. Its ability to invade nonphagocytic cells, evading the immune system and persisting intracellularly complicates the treatment and contributes to recurrent infections. In this study, we investigated the role of cytokines in inhibiting <i>S. aureus</i> adherence and invasion into nonphagocytic human cells. Monomac-6 cells were stimulated with heat-killed <i>S. aureus</i> (HKSA) to produce a cytokine cocktail, which was used to treat various human cell lines, including HEK293, A549, HaCaT, and HT29. Our results demonstrate that cytokines significantly reduced <i>S. aureus</i> adherence and invasion into HEK293, HaCaT, and HT29 cells by altering the expression of key host cell receptors for <i>S. aureus</i> adhesins and invasion, such as integrins and heat shock proteins. These effects of cytokines were mediated via JAK-STAT pathway as tofacitinib supplementation, a JAK inhibitor, reversed the effects of cytokine cocktail. However, these effects were not observed in A549 cells, most likely due to their ability to actively internalize pathogens. These findings suggest that cytokines provide a crucial line of defense against the ability of <i>S. aureus</i> to invade nonphagocytic cells by modulating the expression of host cells receptors.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Cytokine-mediated inhibition of Staphylococcus aureus adherence and invasion into nonphagocytic cells

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年6月20日

查看全文
  • Arif Luqman,
  • Knut Ohlsen

摘要

Staphylococcus aureus is a major pathogen responsible for a wide range of infections, from minor skin diseases to life-threatening conditions, such as sepsis and pneumonia. Its ability to invade nonphagocytic cells, evading the immune system and persisting intracellularly complicates the treatment and contributes to recurrent infections. In this study, we investigated the role of cytokines in inhibiting S. aureus adherence and invasion into nonphagocytic human cells. Monomac-6 cells were stimulated with heat-killed S. aureus (HKSA) to produce a cytokine cocktail, which was used to treat various human cell lines, including HEK293, A549, HaCaT, and HT29. Our results demonstrate that cytokines significantly reduced S. aureus adherence and invasion into HEK293, HaCaT, and HT29 cells by altering the expression of key host cell receptors for S. aureus adhesins and invasion, such as integrins and heat shock proteins. These effects of cytokines were mediated via JAK-STAT pathway as tofacitinib supplementation, a JAK inhibitor, reversed the effects of cytokine cocktail. However, these effects were not observed in A549 cells, most likely due to their ability to actively internalize pathogens. These findings suggest that cytokines provide a crucial line of defense against the ability of S. aureus to invade nonphagocytic cells by modulating the expression of host cells receptors.