Decreased microRNA‑140‑5p contributes to respiratory syncytial virus disease through targeting Toll‑like receptor 4

Abstract

Abstract. The abnormal expression of miRNAs (miRs) has previously been reported in respiratory syncytial virus (RSV) disease. However, to the best of our knowledge, the expression of miR-140-5p in patients with an RSV infection has never been explored. Reverse transcription-quantitative polymerase chain reaction was performed to analyze the level of miR-140-5p in the blood and nasopharyngeal airway samples. ELISAs were performed to determine the levels of tumor necrosis factor α, interleukin (IL)-1β, IL-6 and IL-8. A dual luciferase reporter assay was also performed to investigate the possible target gene of miR-140-5p. The results demonstrated that the levels of miR-140-5p were significantly decreased in the nasal mucosal and peripheral blood samples of patients with RSV infection. It was also revealed that overexpression of miR-140-5p decreased the inflammatory responses, while inhibition of miR-140-5p enhanced the inflammatory responses. Additionally, three binding sites of miR-140-5p in the 3'untranslated region (UTR) of Toll-like receptor (TLR)4 were identified and a dual luciferase reporter assay demonstrated that miR-140-5p significantly suppressed the relative luciferase activity of pmirGLO-TLR4-3'UTR. Furthermore, the level of miR-140-5p was shown to be increased following interferon (IFN)α incubation. Notably, inhibition of miR-140-5p markedly attenuated IFNα-mediated downregulation of tumor necrosis factor α, and interleukin-1β, -6 and -8 in BEAS-2B cells. In summary, decreased miR-140-5p levels are involved in RSV-infection diseases primarily through targeting TLR4.

Silibinin suppresses epithelial–mesenchymal transition in human non-small cell lung cancer cells by restraining RHBDD1

“…Emerging evidence indicates that silencing RHBDD1 suppresses cell growth and proliferation in hepatocellular carcinoma [13], glioblastoma [14] and colorectal cancer [15]. In breast cancer [16,17] and colorectal cancer cells [18], RHBDD1 has been shown to promote migration, invasion and EMT. However, there are few reports on the impact of RHBDD1 on the EMT of NSCLC cells and the associated mechanisms.…”

Immune-related miRNA-mRNA regulation network in the livers of DHAV-3-infected ducklings

“…Meanwhile, the negative miRNA-mRNA network revealed 12 significantly down-regulated miRNAs targeting these TLRs. It has been reported that some miRNAs, like miR-140-5p and welldescribed miR-155, could target TLRs to regulate the innate immune response during the virus infection that had subsequent impact on virus replication [38][39][40]. Upon recognition of pathogens, TLRs recruit a specific set of adaptor molecules, such as MyD88 (myeloid differentiation factor 88) and TIRAP, then initiate downstream signaling events that leads to the secretion of inflammatory cytokines, type I IFN, chemokines, and antimicrobial peptides [41].…”

Immune-related miRNA-mRNA regulation network in the livers of DHAV-3-infected ducklings

“…Meanwhile, the negative miRNA-mRNA network revealed 12 significantly down-regulated miRNAs targeting these TLRs. It has been reported that some miRNAs, like miR-140-5p and well-described miR-155, could target TLRs to regulate the innate immune response during the virus infection that had subsequent impact on virus replication [38][39][40]. Upon recognition of pathogens, TLRs recruit a specific set of adaptor molecules, such as MyD88 (myeloid differentiation factor 88) and TIRAP, then initiate downstream signaling events that leads to the secretion of inflammatory cytokines, type I IFN, chemokines, and antimicrobial peptides [41].…”