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Purpose <p>The autophagy process is critical for cell survival, homeostasis, and functions. Autophagy deregulation was linked to several liver diseases; however, little is known about autophagy status during schistosomiasis and praziquantel (PZQ) treatment. This study is exploring autophagy status during schistosomiasis and praziquantel treatment in the hepatocytes, macrophages, and hepatic stellate cells (HSCs) in mice, and linking the variations in these levels to the parasitic parameters.</p> Methods <p>CD-1 Swiss female albino mice were allocated into three groups: negative control, <i>Schistosoma mansoni</i> (<i>S. mansoni</i>)-infected, and the third group was <i>S. mansoni-</i>infected and treated with PZQ. Liver sections were stained for autophagy markers (LC3 and P62) by immunohistochemistry.</p> Results <p>At 12 weeks post infection, P62 increased in <i>S. mansoni</i>-infected mice in hepatocytes, macrophages, and HSCs compared to negative controls (<i>P</i> = 0.038, <i>P</i> &lt; 0.001, <i>P</i> = 0.004, respectively) and decreased in PZQ-treated group compared to <i>S. mansoni</i>-infected mice in hepatocytes and macrophages only (<i>P</i> &lt; 0.001, <i>P</i> = 0.004, respectively). LC3 displayed higher levels in <i>S. mansoni-</i>infected mice compared to negative controls in hepatocytes, macrophages, and HSCs (<i>P</i> = 0.01, <i>P</i> &lt; 0.001, <i>P</i> &lt; 0.001, respectively), while in PZQ-treated group, it decreased in macrophages and HSCs compared to <i>S. mansoni</i>-infected mice (<i>P</i> = 0.016, <i>P</i> &lt; 0.001, respectively). Correlations were found between the number of eggs and autophagy status, mostly in HSCs.</p> Conclusion <p>Schistosomiasis inhibits autophagy in hepatocytes, macrophages, and HSCs, while PZQ treatment reverses autophagy levels in hepatocytes and macrophages, but not in HSCs. More research is needed to understand the autophagy behavior in HSCs during different stages of schistosomiasis to promote development of autophagy-based anti-fibrotic drugs.</p>

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Autophagic Response of the Liver Cells to Schistosoma mansoni Infection and Praziquantel Treatment

  • 期刊论文

  • 发表日期：

    2025年6月2日

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  • Samar Habib,
  • Heba Hany,
  • Manal Elzoheiry,
  • Manar S. Elmehankar,
  • Suzan H. Elgendy,
  • Emadeldeen Hussin,
  • Khaled Elmasry,
  • Wafaa A. Aboukamar

摘要

Purpose

The autophagy process is critical for cell survival, homeostasis, and functions. Autophagy deregulation was linked to several liver diseases; however, little is known about autophagy status during schistosomiasis and praziquantel (PZQ) treatment. This study is exploring autophagy status during schistosomiasis and praziquantel treatment in the hepatocytes, macrophages, and hepatic stellate cells (HSCs) in mice, and linking the variations in these levels to the parasitic parameters.

Methods

CD-1 Swiss female albino mice were allocated into three groups: negative control, Schistosoma mansoni (S. mansoni)-infected, and the third group was S. mansoni-infected and treated with PZQ. Liver sections were stained for autophagy markers (LC3 and P62) by immunohistochemistry.

Results

At 12 weeks post infection, P62 increased in S. mansoni-infected mice in hepatocytes, macrophages, and HSCs compared to negative controls (P = 0.038, P < 0.001, P = 0.004, respectively) and decreased in PZQ-treated group compared to S. mansoni-infected mice in hepatocytes and macrophages only (P < 0.001, P = 0.004, respectively). LC3 displayed higher levels in S. mansoni-infected mice compared to negative controls in hepatocytes, macrophages, and HSCs (P = 0.01, P < 0.001, P < 0.001, respectively), while in PZQ-treated group, it decreased in macrophages and HSCs compared to S. mansoni-infected mice (P = 0.016, P < 0.001, respectively). Correlations were found between the number of eggs and autophagy status, mostly in HSCs.

Conclusion

Schistosomiasis inhibits autophagy in hepatocytes, macrophages, and HSCs, while PZQ treatment reverses autophagy levels in hepatocytes and macrophages, but not in HSCs. More research is needed to understand the autophagy behavior in HSCs during different stages of schistosomiasis to promote development of autophagy-based anti-fibrotic drugs.