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<p>Fungal dysbiosis can be associated with the carcinogenesis of malignant tumors, and recent studies have indicated that <i>Aspergillus sydowii</i> (<i>A. sydowii</i>) plays a role in the pathogenesis of lung adenocarcinoma (LUAD). However, current research lacks effective treatment options for LUAD infected with <i>A. sydowii</i>. Therefore, the aim of this study was to investigate the therapeutic effects and mechanisms of β-ionone. Lewis lung cancer (LLC) cell xenograft tumor mouse model was constructed, and <i>A. sydowii</i> or various concentrations of β-ionone were treated. Subsequently, tumor volume and mass were monitored. Fluorescence in situ hybridization (FISH) staining with the D223 28S rRNA probe was employed to assess the abundance of fungi within the tumors. Additionally, immunohistochemical staining, flow cytometry, and ELISA were utilized to analyze the function of myeloid-derived suppressor cells (MDSCs) within the tumor. This study revealed that compared to the control group, <i>A. sydowii</i>-infected mice exhibited significantly increased tumor volume and mass (<i>P</i> &lt; 0.001), enhanced Ki-67 staining intensity in tumor tissues (<i>P</i> &lt; 0.01), and elevated fungal abundance within the tumor microenvironment (<i>P</i> &lt; 0.001). Furthermore, <i>A. sydowii</i> promoted the expansion and functional activation of CD11b<sup>+</sup> Gr1<sup>+</sup> MDSCs. In contrast, β-ionone treatment suppressed LUAD tumor growth while concurrently inhibiting MDSC functional activation. Mechanistic investigations demonstrated that β-ionone exerts its anti-tumor and anti-fungal effects by suppressing the activation of the CARD9/p38 MAPK signaling pathway. β-ionone exhibits antitumor activity in <i>A. sydowii</i>-induced LUAD, which supports the potential clinical application of β-ionone in lung cancer therapy.</p>

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β-Ionone inhibits A. sydowii mediated LUAD progression by inhibiting myeloid-derived suppressor cell (MDSC) expansion and activation

  • 期刊论文

  • 发表日期：

    2026年1月12日

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  • Xiaoping Liu,
  • Shuhua Li,
  • Keyi Chen,
  • Xue Yang,
  • Yanxia Yang,
  • Xin Wang

摘要

Fungal dysbiosis can be associated with the carcinogenesis of malignant tumors, and recent studies have indicated that Aspergillus sydowii (A. sydowii) plays a role in the pathogenesis of lung adenocarcinoma (LUAD). However, current research lacks effective treatment options for LUAD infected with A. sydowii. Therefore, the aim of this study was to investigate the therapeutic effects and mechanisms of β-ionone. Lewis lung cancer (LLC) cell xenograft tumor mouse model was constructed, and A. sydowii or various concentrations of β-ionone were treated. Subsequently, tumor volume and mass were monitored. Fluorescence in situ hybridization (FISH) staining with the D223 28S rRNA probe was employed to assess the abundance of fungi within the tumors. Additionally, immunohistochemical staining, flow cytometry, and ELISA were utilized to analyze the function of myeloid-derived suppressor cells (MDSCs) within the tumor. This study revealed that compared to the control group, A. sydowii-infected mice exhibited significantly increased tumor volume and mass (P < 0.001), enhanced Ki-67 staining intensity in tumor tissues (P < 0.01), and elevated fungal abundance within the tumor microenvironment (P < 0.001). Furthermore, A. sydowii promoted the expansion and functional activation of CD11b+ Gr1+ MDSCs. In contrast, β-ionone treatment suppressed LUAD tumor growth while concurrently inhibiting MDSC functional activation. Mechanistic investigations demonstrated that β-ionone exerts its anti-tumor and anti-fungal effects by suppressing the activation of the CARD9/p38 MAPK signaling pathway. β-ionone exhibits antitumor activity in A. sydowii-induced LUAD, which supports the potential clinical application of β-ionone in lung cancer therapy.