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<p>Visceral leishmaniasis (VL) is transmitted by <i>Leishmania</i>-infected sand fly bites and malnutrition is a known risk factor in human VL. Models using sand fly transmission or malnutrition promote parasite dissemination. By investigating features of <i>L. donovani</i>-<i>Lutzomyia longipalpis</i> transmission to malnourished mice, we show that a comparable IL1-β-driven acute inflammation is maintained in malnourished (MN-SF) and well-nourished (WN-SF) sand fly-infected mice. However, parasite dissemination was more pronounced in MN-SF that had a significantly higher acute (<i>P</i> ≤ 0.001) and chronic (<i>P</i> ≤ 0.0001) splenic parasite burden compared to WN-SF. Compared to WN-SF, MN-SF exhibited chronic clinical symptoms (<i>P</i> ≤ 0.0001), neutrophilia (<i>P</i> ≤ 0.001), lymphocytopenia (<i>P</i> ≤ 0.0001), increased heme oxygenase-1 (<i>P</i> ≤ 0.001) and IL17-A (<i>P</i> ≤ 0.0001) levels, dysregulation of liver enzymes, lymph node barrier dysfunction, and augmented dysbiosis, all associated with enhanced VL severity. Combining vector-transmission and malnutrition provides an improved model to study VL pathogenesis and host defense.</p>

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Malnutrition exacerbates pathogenesis of Lutzomyia longipalpis sand fly-transmitted Leishmania donovani

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年5月13日

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  • Eva Iniguez,
  • Johannes Doehl,
  • Pedro Cecilio,
  • Tiago Donatelli Serafim,
  • Caroline Percopo,
  • Yvonne Rangel-Gonzalez,
  • Somaditya Dey,
  • Elvia J. Osorio,
  • Patrick Huffcutt,
  • Sofia Roitman,
  • Claudio Meneses,
  • Mara Short,
  • Jesus G. Valenzuela,
  • Peter C. Melby,
  • Shaden Kamhawi

摘要

Visceral leishmaniasis (VL) is transmitted by Leishmania-infected sand fly bites and malnutrition is a known risk factor in human VL. Models using sand fly transmission or malnutrition promote parasite dissemination. By investigating features of L. donovani-Lutzomyia longipalpis transmission to malnourished mice, we show that a comparable IL1-β-driven acute inflammation is maintained in malnourished (MN-SF) and well-nourished (WN-SF) sand fly-infected mice. However, parasite dissemination was more pronounced in MN-SF that had a significantly higher acute (P ≤ 0.001) and chronic (P ≤ 0.0001) splenic parasite burden compared to WN-SF. Compared to WN-SF, MN-SF exhibited chronic clinical symptoms (P ≤ 0.0001), neutrophilia (P ≤ 0.001), lymphocytopenia (P ≤ 0.0001), increased heme oxygenase-1 (P ≤ 0.001) and IL17-A (P ≤ 0.0001) levels, dysregulation of liver enzymes, lymph node barrier dysfunction, and augmented dysbiosis, all associated with enhanced VL severity. Combining vector-transmission and malnutrition provides an improved model to study VL pathogenesis and host defense.