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Volume 13
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10.3390/microorganisms13030531
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Article

Itaconate: A Nexus Metabolite Fueling Leishmania Survival Through Lipid Metabolism Modulation

by
Ayyoub Kihel
1,†,
Hajar El Filaly
1,†,
Dounia Darif
1,
Aicha Assouab
1,
Myriam Riyad
2,
Imane Nait Irahal
1 and
Khadija Akarid
1,*
1
Biochemistry, Biotechnology and Immunophysiopathology Research Team, Health and Environment Laboratory, Ain Chock Faculty of Sciences, Hassan II University of Casablanca (UH2C), Casablanca 20100, Morocco
2
Immunopathology of Infectious and Systemic Diseases, Laboratory of Cellular and Molecular Pathology, Faculty of Medicine and Pharmacy, Hassan II University of Casablanca (UH2C), Casablanca 20000, Morocco
*
Author to whom correspondence should be addressed.
†
These authors contributed equally to this work.
Microorganisms 2025, 13(3), 531; https://doi.org/10.3390/microorganisms13030531
Submission received: 22 January 2025 / Revised: 21 February 2025 / Accepted: 25 February 2025 / Published: 27 February 2025
(This article belongs to the Special Issue Antileishmanial Agents)
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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 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.
Keywords: Leishmania; itaconate; Acod1; IL1b; Ldlr; Src; Hadh; M1/M2 macrophages Leishmania; itaconate; Acod1; IL1b; Ldlr; Src; Hadh; M1/M2 macrophages

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MDPI and ACS Style

Kihel, A.; El Filaly, H.; Darif, D.; Assouab, A.; Riyad, M.; Nait Irahal, I.; Akarid, K. Itaconate: A Nexus Metabolite Fueling Leishmania Survival Through Lipid Metabolism Modulation. Microorganisms 2025, 13, 531. https://doi.org/10.3390/microorganisms13030531

AMA Style

Kihel A, El Filaly H, Darif D, Assouab A, Riyad M, Nait Irahal I, Akarid K. Itaconate: A Nexus Metabolite Fueling Leishmania Survival Through Lipid Metabolism Modulation. Microorganisms. 2025; 13(3):531. https://doi.org/10.3390/microorganisms13030531

Chicago/Turabian Style

Kihel, Ayyoub, Hajar El Filaly, Dounia Darif, Aicha Assouab, Myriam Riyad, Imane Nait Irahal, and Khadija Akarid. 2025. "Itaconate: A Nexus Metabolite Fueling Leishmania Survival Through Lipid Metabolism Modulation" Microorganisms 13, no. 3: 531. https://doi.org/10.3390/microorganisms13030531

APA Style

Kihel, A., El Filaly, H., Darif, D., Assouab, A., Riyad, M., Nait Irahal, I., & Akarid, K. (2025). Itaconate: A Nexus Metabolite Fueling Leishmania Survival Through Lipid Metabolism Modulation. Microorganisms, 13(3), 531. https://doi.org/10.3390/microorganisms13030531

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