Respiratory syncytial virus infection inhibits TLR4 signaling via up‐regulation of miR‐26b

Liu, Shuang; Gao, Li; Wang, Xia; Xing, Yan

doi:10.1002/cbin.10518

Cited by 18 publications

(17 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A previous study revealed that RSV infection enhances the airway epithelial cell receptors, which may enhance the binding of inhaled environmental agents (26). The current study revealed that the level of TLR4 was increased by ~1.67-, ~2.56-and ~3.89-fold in RSV infected cells at 6, 12 and 24 h, respectively.…”

Section: Discussionsupporting

confidence: 52%

LncRNA MEG3 ameliorates respiratory syncytial virus infection by suppressing TLR4 signaling

et al. 2017

View full text Add to dashboard Cite

Maternally expressed gene 3 (MEG3), a long noncoding RNA (lncRNA) has been dysregulated in various tumors. However, the expression level and functional role of MEG3 in the progression of respiratory syncytial virus (RSV) infection remains to be elucidated. The present study quantified the expression level of MEG3 in the nasopharyngeal (NPA) samples of RSV‑infected patients and in BEAS‑2B cells infected with RSV. The findings of the present study demonstrated that the expression level of lncRNA MEG3 was reduced in the NPA samples of RSV‑infected patients and in BEAS‑2B cells infected with RSV. In vitro transfection revealed increased mRNA expression levels of toll‑like receptor 4 (TLR4), tumor necrosis factor‑α (TNFα) and interleukin (IL)‑8 following RSV infection in BEAS‑2B cells. Additionally, ectopic expression of MEG3 reduced the expression level of TLR4, subsequently suppressing the mRNA expression levels of TNFα and IL‑8, indicating the protective role of MEG3 in the process of RSV infection. It is of note, that RSV infection‑induced p38 mitogen activated protein kinase (MAPK) and nuclear factor‑κB (NF‑κB) activation was partly abolished by overexpression of MEG3. In conclusion, to the best of our knowledge, the present study provided the first evidence that lncRNA MEG3 expression level was reduced in the NPA samples of patients with RSV infection and RSV‑infected cells. Additionally, it was demonstrated that MEG3 protected human airway epithelial cells from RSV infection, primarily by suppressing TLR4‑dependent p38 MAPK and NF‑κB signaling.

show abstract

Section: Discussionsupporting

confidence: 52%

LncRNA MEG3 ameliorates respiratory syncytial virus infection by suppressing TLR4 signaling

et al. 2017

View full text Add to dashboard Cite

show abstract

“…miR-125a and miR-429 are downregulated in mild but not severe infection; the former has roles in NF-B signaling and macrophage function (162). miR-26b (which is thought to target TLR4 based on miRNA target prediction software) has been studied in PBMCs from children with RSV bronchiolitis, where it is upregulated, negatively correlating with TLR4 expression (163).…”

Section: Innate Interferonsmentioning

confidence: 99%

The Human Immune Response to Respiratory Syncytial Virus Infection

et al. 2017

View full text Add to dashboard Cite

Respiratory syncytial virus (RSV) is an important etiological agent of respiratory infections, particularly in children. Much information regarding the immune response to RSV comes from animal models and studies. Here, we provide a comprehensive description of the human immune response to RSV infection, based on a systematic literature review of research on infected humans. There is an initial strong neutrophil response to RSV infection in humans, which is positively correlated with disease severity and mediated by interleukin-8 (IL-8). Dendritic cells migrate to the lungs as the primary antigen-presenting cell. An initial systemic T-cell lymphopenia is followed by a pulmonary CD8 T-cell response, mediating viral clearance. Humoral immunity to reinfection is incomplete, but RSV IgG and IgA are protective. B-cell-stimulating factors derived from airway epithelium play a major role in protective antibody generation. Gamma interferon (IFN-γ) has a strongly protective role, and a Th2-biased response may be deleterious. Other cytokines (particularly IL-17A), chemokines (particularly CCL-5 and CCL-3), and local innate immune factors (including cathelicidins and IFN-λ) contribute to pathogenesis. In summary, neutrophilic inflammation is incriminated as a harmful response, whereas CD8 T cells and IFN-γ have protective roles. These may represent important therapeutic targets to modulate the immunopathogenesis of RSV infection.

show abstract

“…In vitro , miR-26b mimic markedly down-regulated TLR4 mRNA/protein expression and IFNB/CCL5 concentrations, while miR-26b inhibitor up-regulated these levels. Therefore, RSV infection inhibits TLR4 signaling via up-regulation of miR-26b, which provides a potential therapeutic target for preventing and treating RSV infection 99. In whole blood samples from RSV-infected infants, it was found that miR-106b-5p, miR-20b-5p, and miR-342-3p were upregulated with RSV infection, while miR-320e, miR-320d, miR-877-5p, miR-122-5p and miR-92b-5p were down-regulated.…”

Section: Virus-induced Mirs Profiles In Pbmcsmentioning

confidence: 99%

MicroRNAs in Asthma and Respiratory Infections: Identifying Common Pathways

Τaka

Tzani-Tzanopoulou

Wanstall

et al. 2020

Allergy Asthma Immunol Res

View full text Add to dashboard Cite

MicroRNAs (miRs) are single-stranded RNAs of 18-25 nucleotides. These molecules regulate gene expression at the post-transcriptional level; several of these are differentially expressed in asthma as well as in viral acute respiratory infections (ARIs), the main triggers of acute asthma exacerbations. In recent years, miRs have been studied in order to discover drug targets as well as biomarkers for diagnosis, disease severity and prognosis. We describe recent findings on miR expression and function in asthma and their role in the regulation of viral ARIs, according to cell tissue specificity and asthma severity. By combining the above information, we identify miRs that may be important in virus-induced asthma exacerbations. This is the first attempt to link miR profiles of asthmatic patients and ARI-induced miRs, addressing the question of whether there might be a specific miR deficit in asthmatic subjects that make them more susceptible and/or reactive to infection.

show abstract

Respiratory syncytial virus infection inhibits TLR4 signaling via up‐regulation of miR‐26b

Cited by 18 publications

References 29 publications

LncRNA MEG3 ameliorates respiratory syncytial virus infection by suppressing TLR4 signaling

LncRNA MEG3 ameliorates respiratory syncytial virus infection by suppressing TLR4 signaling

The Human Immune Response to Respiratory Syncytial Virus Infection

MicroRNAs in Asthma and Respiratory Infections: Identifying Common Pathways

Contact Info

Product

Resources

About