The expression profile of inflammatory microRNAs in Leishmania major infected human macrophages; mining the effects of Leishmania RNA virus

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 patte...

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Main Authors: Zahra Mirabedini, Mehdi Mohebali, Hamed Mirjalali, Homa Hajjaran, Fatemeh Goudarzi, Hanieh Mohammad Rahimi
Format: Article
Language:English
Published: BMC 2025-04-01
Series:BMC Microbiology
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Online Access:https://doi.org/10.1186/s12866-025-03901-z
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Summary: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.
ISSN:1471-2180