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Leishmania survives by exporting miR-146a from infected to resident cells to subjugate inflammation

Satarupa Ganguly1, Bartika Ghoshal1, Ishani Banerji1,2

  • 1RNA Biology Research Laboratory, Molecular Genetics Division, Council of Scientific and Industrial Research (CSIR)-Indian Institute of Chemical Biology, Kolkata, India.

Life Science Alliance
|February 25, 2022
PubMed

Insights

Leishmania donovani manipulates host microRNAs (miRNAs) to control inflammation during visceral leishmaniasis. Infected cells export miR-146a to suppress inflammation and promote M2 macrophage polarization, aiding parasite survival.

Area of Science:

  • Parasitology
  • Immunology
  • Molecular Biology

Background:

  • Leishmania donovani causes visceral leishmaniasis by infecting macrophages.
  • The communication between infected and non-infected cells in regulating infection is not well understood.
  • Parasite survival strategies involve manipulating host cellular processes.

Purpose of the Study:

  • To elucidate the role of intercellular miRNA transport in Leishmania donovani infection.
  • To understand how infected cells regulate host inflammatory responses via miRNA exchange.
  • To investigate the mechanisms by which Leishmania donovani manipulates host miRNA profiles for its survival.

Main Methods:

  • Analysis of extracellular vesicle-mediated miRNA transfer between host cells.
  • Investigation of host cell mitochondrial function in response to infection.
  • Assessment of miRNA expression and function in infected and non-infected cells.
  • Macrophage polarization assays (M1/M2) and cytokine expression analysis.

Main Results:

  • Leishmania donovani prevents mitochondrial dysfunction to restrict miR-122 entry into infected macrophages, limiting inflammation.
  • The parasite up-regulates the export of miR-146a from infected cells via extracellular vesicles.
  • miR-146a restricts miR-122 production in hepatocytes and polarizes neighboring macrophages to the M2 state.
  • In recipient macrophages, miR-146a inhibits pro-inflammatory cytokine production and up-regulates IL-10 by promoting miR-21 export, inducing M2 polarization.

Conclusions:

  • Leishmania donovani employs a dual miRNA strategy to evade host immunity and promote survival.
  • Intercellular miRNA transport is a critical mechanism for parasite-induced immune modulation.
  • Targeting host miRNA pathways represents a potential therapeutic strategy for visceral leishmaniasis.

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