Related Experiment Video
Updated: Jan 18, 2026
Investigating the Phagocytosis of Leishmania using Confocal Microscopy
Published on: July 29, 2021
Expression of Cytokine Signaling Pathway Related Genes in Leishmania-infected Macrophages
Ufuk Mert1, Hamid Alizadeh2, Can Müftüoğlu3
1Ege University, Atatürk Vocational School of Health Services, İzmir, Türkiye.
Objective:
Leishmaniasis, caused by protozoan parasites of the Leishmania spp., presents significant global health challenges, with visceral leishmaniasis (VL) and cutaneous leishmaniasis forms causing severe morbidity and mortality. Macrophages serve as primary host cells, where Leishmania spp. modulate immune 30 responses to ensure survival. Our study investigated gene expression changes in THP1-derived macrophages infected with L. infantum and L. tropica to elucidate host-pathogen interactions.
Methods:
Macrophages were infected with stationary-phase promastigotes, and infection rates were confirmed via Giemsa staining. RNA was extracted, and real time-quantitative polymerase chain reaction was performed to analyze the expression of immune-related genes (STAT1, STAT2, CCL4, IL23A, IL1R1, IL1RN).
Results:
Results demonstrated significant upregulation of STAT1 and STAT2, key mediators of the JAK-STAT pathway, in both infections, aligning with prior in vivo and in vitro studies. CCL4, a chemokine linked to macrophage recruitment, was also elevated, consistent with findings in VL and canine leishmaniasis. IL23A, associated with Th17 responses, showed increased expression, supporting its role in leishmanial immune modulation. Notably, IL1RN, an anti-inflammatory mediator, was upregulated, 40 suggesting a balancing mechanism to prevent excessive inflammation.
Conclusion:
These findings highlight the complex interplay between pro- and anti-inflammatory responses during Leishmania infection and underscore potential targets for diagnostic and therapeutic strategies.
Insights
Leishmania parasites infect macrophages, altering immune gene expression. This study reveals complex pro- and anti-inflammatory responses, offering insights into leishmaniasis diagnostics and therapies.
Area of Science:
- Immunology
- Parasitology
- Molecular Biology
Background:
- Leishmaniasis poses a global health threat, caused by Leishmania parasites.
- Macrophages are key host cells targeted by Leishmania, which manipulates immune responses.
- Visceral leishmaniasis (VL) and cutaneous leishmaniasis cause significant morbidity and mortality.
Purpose of the Study:
- Investigate gene expression changes in macrophages infected with Leishmania infantum and Leishmania tropica.
- Elucidate host-pathogen interactions at the molecular level.
- Identify potential diagnostic and therapeutic targets for leishmaniasis.
Main Methods:
- Infection of THP1-derived macrophages with Leishmania promastigotes.
- Confirmation of infection rates using Giemsa staining.
- Real-time quantitative PCR analysis of immune-related genes (STAT1, STAT2, CCL4, IL23A, IL1R1, IL1RN).
Main Results:
- Significant upregulation of STAT1 and STAT2, involved in the JAK-STAT pathway.
- Elevated CCL4 expression, indicating macrophage recruitment.
- Increased IL23A (Th17 response) and IL1RN (anti-inflammatory) suggest immune modulation.
Conclusions:
- Leishmania infection triggers complex pro- and anti-inflammatory responses in macrophages.
- Gene expression patterns highlight the intricate host-pathogen interplay.
- Findings suggest potential avenues for leishmaniasis diagnostics and therapeutics.
