Antileishmanial Agents

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Molecular Microbiology and Immunology".

Deadline for manuscript submissions: 31 August 2025 | Viewed by 672

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Guest Editor
Laboratório de Farmacologia e Bioquímica (LFBq), Departamento de Medicina Veterinária, Faculdade de Zootecnia e Engenharia de Alimentos, Universidade de São Paulo, Pirassununga 13635-900, SP, Brazil
Interests: pathogen biochemistry and pharmacology; neglected disease (leishmaniasis); drug development
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Special Issue Information

Dear Colleagues,

Leishmaniasis, a neglected tropical disease transmitted by sandflies, inflicts a substantial global health burden, particularly in tropical and subtropical regions. The intricate life cycle of Leishmania parasites, alternating between insect vectors and mammalian hosts, poses significant challenges in disease control and treatment. To combat this pressing health concern, fostering collaborative research to elucidate the parasite's physiology, biochemistry, and regulatory pathways is imperative. A deeper understanding of these mechanisms is crucial for identifying novel drug targets and designing efficacious therapies.

This Special Issue seeks to provide a platform for disseminating high-quality reviews and original research articles that propel advancements in leishmaniasis drug discovery. The scope encompasses a broad spectrum of topics related to drug target identification, drug design, and model testing. We especially welcome submissions that employ cutting-edge approaches, such as high-throughput screening, molecular docking, and structure-based drug design.

By showcasing innovative research from scientists worldwide, this Special Issue aspires to accelerate the development of novel and enhanced pharmaceutical interventions against leishmaniasis. We anticipate that the published works will not only stimulate further research endeavors but also contribute significantly to the ultimate goal of realizing new therapeutic strategies for this disease.

You may choose our Joint Special Issue in Microbiology Research.

Dr. Edson Roberto da Silva
Guest Editor

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Keywords

  • leishmaniasis
  • Leishmania
  • drug discovery
  • pharmaceutical interventions
  • therapeutic strategies

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Published Papers (1 paper)

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Research

12 pages, 1188 KiB  
Article
Itaconate: A Nexus Metabolite Fueling Leishmania Survival Through Lipid Metabolism Modulation
by Ayyoub Kihel, Hajar El Filaly, Dounia Darif, Aicha Assouab, Myriam Riyad, Imane Nait Irahal and Khadija Akarid
Microorganisms 2025, 13(3), 531; https://doi.org/10.3390/microorganisms13030531 - 27 Feb 2025
Viewed by 431
Abstract
Leishmaniasis, caused by the Leishmania parasite, is a neglected public health issue. Leishmania mainly infects macrophages, where metabolic reprogramming shapes their plasticity (M1/M2), affecting the host’s resistance or susceptibility to infection. The development of this infection is influenced by immune responses, with an [...] Read more.
Leishmaniasis, caused by the Leishmania parasite, is a neglected public health issue. Leishmania mainly infects macrophages, where metabolic reprogramming shapes their plasticity (M1/M2), affecting the host’s resistance or susceptibility to infection. The development of this infection is influenced by immune responses, with an excessive anti-inflammatory reaction linked to negative outcomes through the modulation of various mediators. Itaconate, produced by the Acod1 gene, is recognized for its anti-inflammatory effects, but its function in leishmaniasis is not well understood. This study aimed to investigate the potential role of itaconate in leishmaniasis. Using transcriptomic data from L. major-infected BMDMs, we assessed the expression dynamics of Il1b and Acod1 and performed pathway enrichment analysis to determine the profile of genes co-expressed with Acod1. Early Acod1 upregulation followed by later Il1b downregulation was noted, indicating a shift towards an anti-inflammatory response. Among the genes co-expressed with Acod1, Ldlr, Hadh, and Src are closely associated with lipid metabolism and the polarization of macrophages towards the M2 phenotype, thereby creating a favorable environment for the survival of Leishmania. Overall, these findings suggest that Acod1 and its co-expressed genes may affect the outcome of Leishmania infection by modulating host metabolism. Accordingly, targeting itaconate-associated pathways could provide a novel therapeutic strategy for leishmaniasis. Full article
(This article belongs to the Special Issue Antileishmanial Agents)
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