Turkiye parazitolojii dergisi · 2025
Expression of Cytokine Signaling Pathway Related Genes in Leishmania-infected Macrophages.
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Mert Ufuk, Alizadeh Hamid, Müftüoğlu Can, Caner Ayşe
Аннотация
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.
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.