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<p>Aspiration Pneumonia (AP) is a common disease that can lead to patient mortality, particularly among the elderly population, making it a significant concern in critical care medicine and basic medical research. At present, studies on the pathogenesis of AP have revealed the roles of multiple cytokines and signaling pathways in AP and lung injury. However, research exploring the pathogenesis of AP using transcriptomic sequencing and analysis methods remains limited. This study established an AP animal model and investigated the mechanisms underlying the onset and progression of AP by performing transcriptomic sequencing, bioinformatics analysis, and immune infiltration analysis on rat lung tissues. Our findings revealed that the hub genes <i>Ccl3</i>, <i>Ccl20</i>, <i>Cxcl2</i>, and <i>Tlr1</i> are involved in biological processes such as chemokine activation, inflammatory responses, and immune responses during the pathogenesis of AP. By constructing a ceRNA network, we found the circRNA_18683-rno-miR-128-3p-<i>Cxcl2</i> pathway may play a crucial regulatory role in the pathogenesis of AP. Further immune infiltration analysis showed a possible increase in M0 macrophages and a decrease in Treg cells and mast cells. Targeting these hub genes and cells may represent a potential therapeutic strategy for AP.</p>

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Construction of circRNA-mediated ceRNA network and immunoassay for investigating pathogenesis of aspiration pneumonia

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月24日

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  • Zhiwen Zheng,
  • Zuan Zhan,
  • Yuanyuan Gu,
  • Qiao Wang,
  • Qinrong Zheng,
  • Liang Huang,
  • Jianwen Ding

摘要

Aspiration Pneumonia (AP) is a common disease that can lead to patient mortality, particularly among the elderly population, making it a significant concern in critical care medicine and basic medical research. At present, studies on the pathogenesis of AP have revealed the roles of multiple cytokines and signaling pathways in AP and lung injury. However, research exploring the pathogenesis of AP using transcriptomic sequencing and analysis methods remains limited. This study established an AP animal model and investigated the mechanisms underlying the onset and progression of AP by performing transcriptomic sequencing, bioinformatics analysis, and immune infiltration analysis on rat lung tissues. Our findings revealed that the hub genes Ccl3, Ccl20, Cxcl2, and Tlr1 are involved in biological processes such as chemokine activation, inflammatory responses, and immune responses during the pathogenesis of AP. By constructing a ceRNA network, we found the circRNA_18683-rno-miR-128-3p-Cxcl2 pathway may play a crucial regulatory role in the pathogenesis of AP. Further immune infiltration analysis showed a possible increase in M0 macrophages and a decrease in Treg cells and mast cells. Targeting these hub genes and cells may represent a potential therapeutic strategy for AP.