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<p><i>Listeria monocytogenes</i> is a facultative intracellular pathogen capable of direct intercellular transmission, enabling it to evade extracellular immune defenses and modulate host–pathogen interactions. This study examined the temporal and tissue-specific expression patterns of five genes associated with the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway in the insect host <i>Tenebrio molitor</i> following <i>L. monocytogenes</i> infection. Post-infection, whole body, gut, and Malpighian tubules were dissected at defined time points to assess differential gene expression. A significant induction of multiple JAK/STAT pathway genes was observed across all examined tissues. In whole-body samples, the pathway activator Janus kinase <i>Hopscotch</i> exhibited marked upregulation (&gt; 2 fold) at 12&#xa0;h post-infection, indicating the onset of signaling activity. The regulatory genes <i>SOCS stops</i> (1.5 fold), <i>SP555</i> (2.5 fold), and <i>SOCS box protein-3</i> (&gt; 3 fold) showed early activation at 3&#xa0;h post-infection, suggesting rapid transcriptional modulation. In gut tissues, <i>Hopscotch</i> expression (&gt; 4 fold) increased from 3&#xa0;h post-infection and remained elevated through day 5, whereas <i>SOCS box protein-3</i> exhibited (&gt; 2 fold) the strongest regulatory effect, followed by moderate expression of <i>SOCS stops</i> (max 2 fold) and minimal <i>SP555</i> activity. In Malpighian tubules, <i>Hopscotch</i> (&gt; 2 fold) and the transcription factor <i>Stat92E</i> (&gt; 4 fold) were upregulated from 6&#xa0;h post-infection and remained elevated until day 5. <i>SOCS box protein-3</i> again demonstrated predominant regulatory activity, while <i>SOCS stops</i> and <i>SP555</i> showed no detectable expression. Collectively, these findings indicate that JAK/STAT pathway gene expression in <i>T. molitor</i> during <i>L. monocytogenes</i> infection is both time-dependent and tissue-specific, reflecting a finely tuned immune response to intracellular bacterial invasion.</p>

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Tissue- and time-dependent modulation of JAK/STAT pathway genes in Tenebrio molitor during Listeria monocytogenes infection

  • 期刊论文

  • 发表日期：

    2026年4月10日

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  • Shahidul Ahmed Khan,
  • Ki Beom Park,
  • Yeon Soo Han

摘要

Listeria monocytogenes is a facultative intracellular pathogen capable of direct intercellular transmission, enabling it to evade extracellular immune defenses and modulate host–pathogen interactions. This study examined the temporal and tissue-specific expression patterns of five genes associated with the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway in the insect host Tenebrio molitor following L. monocytogenes infection. Post-infection, whole body, gut, and Malpighian tubules were dissected at defined time points to assess differential gene expression. A significant induction of multiple JAK/STAT pathway genes was observed across all examined tissues. In whole-body samples, the pathway activator Janus kinase Hopscotch exhibited marked upregulation (> 2 fold) at 12 h post-infection, indicating the onset of signaling activity. The regulatory genes SOCS stops (1.5 fold), SP555 (2.5 fold), and SOCS box protein-3 (> 3 fold) showed early activation at 3 h post-infection, suggesting rapid transcriptional modulation. In gut tissues, Hopscotch expression (> 4 fold) increased from 3 h post-infection and remained elevated through day 5, whereas SOCS box protein-3 exhibited (> 2 fold) the strongest regulatory effect, followed by moderate expression of SOCS stops (max 2 fold) and minimal SP555 activity. In Malpighian tubules, Hopscotch (> 2 fold) and the transcription factor Stat92E (> 4 fold) were upregulated from 6 h post-infection and remained elevated until day 5. SOCS box protein-3 again demonstrated predominant regulatory activity, while SOCS stops and SP555 showed no detectable expression. Collectively, these findings indicate that JAK/STAT pathway gene expression in T. molitor during L. monocytogenes infection is both time-dependent and tissue-specific, reflecting a finely tuned immune response to intracellular bacterial invasion.