ArticleBMC microbiology2025
The expression profile of inflammatory microRNAs in Leishmania major infected human macrophages; mining the effects of Leishmania RNA virus.
Article in BMC microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLeishmaniasis 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-.
methodsSamples 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.
resultsThe 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-.
conclusionIn 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.
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