Masoudzadeh N, Ait Kbaich M, van Veen S, Andersson B, C Haks M, Persson J, Mashayekhi Goyonlo V, Hadifar S, Erfanian Salim R, Mhaidi I, Riyad M, Akarid K, M Harandi A, Hm Ottenhoff T, Lemrani M, Rafati S
PLoS Negl Trop Dis 19 (3) e0012812 [2025-03-00; online 2025-03-18]
Cutaneous leishmaniasis (CL) is the most prevalent type of leishmaniasis disease and causes skin lesions, mainly ulcers, on exposed parts of the body. The Americas, Mediterranean basin, Middle East, and Central Asia account for approximately 95% of all CL cases. Leishmania (L.) major and L. tropica are the most significant species causing CL. A better understanding of the molecular mechanisms of CL caused by Leishmania parasite species in patients' skin lesions may help inform intervention approaches. Using dual-color reverse transcriptase multiplex ligation-dependent probe amplification (dcRT-MLPA), we evaluated the expression of 144 host immune-related genes in lesions from CL patients infected with two Leishmania species, L. major and L. tropica, in Morocco and Iran, respectively. Distinct gene expression patterns were identified in the lesions of patients infected with L. major and L. tropica. The results revealed that L. tropica-infected patients had rather more significant gene expression than L. major-infected patients relative to healthy volunteers. However, CD14 and IFI6 (interferon alpha inducible protein 6), were two common genes expressed in the lesions of patients infected with L. major and L. tropica. Our analysis revealed that gene expression changes related to the IFN signaling pathway were significant in both lesion groups. This research advances our understanding of the host immune response to zoonotic and anthroponotic leishmaniasis and shows immune transcript signatures in the skin lesions of CL patients infected with L. major and L. tropica. These findings can inform further investigation into the processes underpinning immunity and immunopathology of CL caused by L. major and L. tropica.
Clinical Genomics [Collaborative]
Clinical Genomics Gothenburg [Collaborative]
PubMed 40100809
DOI 10.1371/journal.pntd.0012812
Crossref 10.1371/journal.pntd.0012812
pmc: PMC11918365
pii: PNTD-D-24-00402