The Expression Profile of Inflammatory Micrornas in Leishmania Major Infected Human Macrophages; Mining the Effects of Leishmania Rna Virus Publisher Pubmed



Mirabedini Z¹ ; Mohebali M^{1, 2} ; Mirjalali H³ ; Hajjaran H¹ ; Goudarzi F¹ ; Rahimi HM³ Show Affiliations
Source: BMC Microbiology Published:2025

Abstract

Background: Leishmaniasis is a disease caused by the Leishmania parasite. Recent studies suggest a critical role for double-stranded RNA virus (LRV) in the disease outcome. MicroRNAs (miRs) are small, non-coding RNA molecules that may also contribute to the outcome of infection and the pattern of disease. This study aimed to investigate the influence of L. major infected with LRV2 + on the expression profile of microRNAs compared to LRV2-. Methods: Samples were collected from cutaneous leishmaniasis (CL) patients in a leishmaniasis-endemic area of Iran. Leishmania species were determined using PCR (kDNA gene), and the presence of LRV2 was identified with semi-nested PCR (RdRp gene). The expression of miRs (miR-155, miR-146b, and miR-133a) was determined through quantitative real-time PCR analysis in human monocytes cell line (THP-1) infected with both LRV2 + and LRV2- isolates of L. major during 0, 12, 24, and 36 h post-co-infection. Results: The expression of miR-155 showed a significant decrease in the LRV2 + isolate compared to LRV2- at zero hours, but exhibited upregulation at 12, 24, and 36 h post-infection for both LRV2 + and LRV2- isolates compared to the control group. The expression of miR-146b was upregulated in both LRV2 + and LRV2- isolates compared to the control group at zero, 24, and 36 h post-infection. Conversely, miR-133a showed significant increases at zero and 12 h in both LRV2 + and LRV2- isolates compared to the control group, but it was downregulated in LRV2 + at 24 and 36 h compared to LRV2-. Conclusion: In this study, significant differences were observed in the expression profiles of miR-155, miR-146b, and miR-133a about the presence of LRV2. Our data suggest a potential determinative role for these miRs in the pathogenesis of CL. © The Author(s) 2025.