ORIGINAL RESEARCH article
Front. Immunol.
Sec. Parasite Immunology
Human macrophages release exosomes containing anti-inflammatory microRNAs after phagocytosis of Leishmania infantum
Provisionally accepted
- 1Department of Internal Medicine, Carver College of Medicine, The University of Iowa, Iowa, Iowa, United States
- 2Department of Microbiology and Immunology, Carver College of Medicine, The University of Iowa, Iowa, Iowa, United States
- 3Iowa City VA Health Care System, Veterans Health Administration, United States Department of Veterans Affairs, Iowa City, Iowa, United States
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The protozoan Leishmania infantum causes visceral leishmaniasis (VL), a disease associated with suppressed systemic innate and adaptive immune responses. Mechanisms underlying the generalized immune suppression are incompletely understood. Exosomes are a subset of microvesicles released from eukaryotic cells, which contain proteins, lipids and nucleic acids including microRNAs (miRNAs). These small regulatory RNAs can simultaneously modify expression of many genes and pathways. We hypothesized that L. infantum infection of macrophages induces release of exosomes containing immunomodulatory miRNAs that contribute to systemic immunosuppression during VL. Using NanoString arrays, we profiled exosomal miRNAs released by infected versus uninfected human macrophages. These revealed differential expression of several miRNAs including hsa-miR-223-3p, which has known anti-inflammatory activities. Target prediction pathways indicated the NLRP3 inflammasome pathway might be targeted by differentially expressed miRNAs, a hypothesis that was confirmed in transfected THP-1 monocytic cells overexpressing hsa-miR-223-3p. We hypothesize that L. infantum infection might induce the release of exosomes containing miRNAs that modify the host immune environment to suppress microbicidal pathways and favor parasite survival.
Keywords: Leishmania infantum, Visceral leishmaniasis, Exosomes, MicroRNAs, Human macrophage
Received: 14 Mar 2025; Accepted: 03 Nov 2025.
Copyright: © 2025 Hudachek, Zhanbolat, Chen and Wilson. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Mary Edythe Wilson, mary-wilson@uiowa.edu
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