The role of miR-155 in cigarette smoke-induced pulmonary inflammation and COPD

Smet, Elise G De; Eeckhoutte, Hannelore P Van; Cobos, Francisco Avila; Blomme, Evy; Verhamme, Fien; Provoost, Sharen; Verleden, Stijn E.; Venken, Koen; Maes, Tania; Joos, Guy; Mestdagh, Pieter; Brusselle, Guy; Bracke, Ken R.

doi:10.1038/s41385-019-0241-6

Cited by 59 publications

(51 citation statements)

References 51 publications

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“…Recent studies have shown that miR-155 knockout (KO) mice have decreased lung inflammation and recover faster from influenza infection [22]. Similarly, cigarette smoke-induced lung inflammation is reduced in miR-155 KO mice and mitigated by anti-miR-155 treatment [23]. Collectively, these data demonstrate that miR-155 has a powerful but unclear role fine-tuning host TH1/ TH2 antiviral immunity.…”

Section: Introductionmentioning

confidence: 85%

“…The importance of these data is that miR-155 is an evolutionarily-conserved molecule with essential but still unclear roles promoting both TH1 antiviral immunity [3][4][5][6][7][8][9][10][11][12], as well as TH2 allergic inflammation [16][17][18][19]. Thus, there is increasing interest in defining the precise role(s) of miR-155 in human airway immunity and in the pathobiology of airway diseases such as COPD [23], asthma [28], and viral respiratory infections in young children [14,15]. Over the past decade many studies have identified that miR-155 is a master regulator of the immune system [1,2].…”

Section: Plos Onementioning

confidence: 99%

“…MiR-155 is also a robust marker of pro-inflammatory responses in different cell systems [20][21][22][23]. There is compelling evidence demonstrating that miR-155 is highly expressed in macrophages, dendritic cells, as well as T and B lymphocytes [1][2][3] and is selectively exported by these cells in exosomes to allow cell-to-cell communication and amplification of pro-inflammatory responses in the lungs [29].…”

Section: Plos Onementioning

confidence: 99%

“…However, there is still an important unresolved paradox for the role of miR-155 during viral respiratory infections. Despite being essential for the generation of host antiviral TH1 immunity [3][4][5][6][7][8][9][10][11][12], miR-155 may also contribute to respiratory disease by enhancing allergic TH2 responses [16][17][18][19] and NFkB-mediated inflammation in macrophages and other bone marrow-derived immune cells [20][21][22][23]. Recent studies have shown that miR-155 knockout (KO) mice have decreased lung inflammation and recover faster from influenza infection [22].…”

Section: Introductionmentioning

confidence: 99%

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Airway mir-155 responses are associated with TH1 cytokine polarization in young children with viral respiratory infections

et al. 2020

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Background MicroRNAs (miRs) control gene expression and the development of the immune system and antiviral responses. MiR-155 is an evolutionarily-conserved molecule consistently induced during viral infections in different cell systems. Notably, there is still an unresolved paradox for the role of miR-155 during viral respiratory infections. Despite being essential for host antiviral TH1 immunity, miR-155 may also contribute to respiratory disease by enhancing allergic TH2 responses and NFkB-mediated inflammation. The central goal of this study was to define how airway miR-155 production is related to TH1, TH2, and proinflammatory cytokine responses during naturally occurring viral respiratory infections in young children. Methods Normalized nasal airway levels of miR-155 and nasal protein levels of IFN-γ, TNF-α, IL-1β, IL-13, IL-4 were quantified in young children (�2 years) hospitalized with viral respiratory infections and uninfected controls. These data were linked to individual characteristics and respiratory disease parameters. Results A total of 151 subjects were included. Increased miR-155 levels were observed in nasal samples from patients with rhinovirus, RSV and all respiratory viruses analyzed. High miR-155 levels were strongly associated with high IFN-γ production, increased airway TH1 cytokine polarization (IFN-γ/IL-4 ratios) and increased pro-inflammatory responses. High airway miR-155 levels were linked to decreased respiratory disease severity in individuals with high airway TH1 antiviral responses.

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Section: Introductionmentioning

confidence: 85%

Section: Plos Onementioning

confidence: 99%

Section: Plos Onementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Airway mir-155 responses are associated with TH1 cytokine polarization in young children with viral respiratory infections

et al. 2020

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“…The proinflammatory effects of miR-155 have been elucidated in asthma, idiopathic pulmonary fibrosis, and cigarette-induced inflammation, suggesting a vital role of miR-155 in lung inflammation. [ 23 – 25 ] However, few studies have examined the role of miR-155 in viral infection. Microarray analysis revealed that miR-155 was induced in influenza-infected mice.…”

Section: Discussionmentioning

confidence: 99%

Down-regulation of miR-155 inhibits inflammatory response in human pulmonary microvascular endothelial cells infected with influenza A virus by targeting sphingosine-1-phosphate receptor 1

Shen

Jiang

Zhao

et al. 2020

Chinese Medical Journal

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Background: Endothelial cells play a key role in the cytokine storm caused by influenza A virus. MicroRNA-155 (miR-155) is an important regulator in inflammation. Its role in the inflammatory response to influenza A infection, however, has yet to be elucidated. In this study, we explored the role as well as the underlying mechanism of miR-155 in the cytokine production in influenza A-infected endothelial cells. Methods: Human pulmonary microvascular endothelial cells (HPMECs) were infected with the influenza A virus strain H1N1. The efficiency of H1N1 infection was confirmed by immunofluorescence. The expression levels of proinflammatory cytokines and miR-155 were determined using real-time polymerase chain reaction. A dual-luciferase reporter assay characterized the interaction between miR-155 and sphingosine-1-phosphate receptor 1 (S1PR1). Changes in the target protein levels were determined using Western blot analysis. Results: MiR-155 was elevated in response to the H1N1 infection in HPMECs (24 h post-infection vs . 0 h post-infection, 3.875 ± 0.062 vs . 1.043 ± 0.013, P = 0.001). Over-expression of miR-155 enhanced inflammatory cytokine production (miR-155 mimic vs . negative control, all P < 0.05 in regard of cytokine levels) and activation of nuclear factor kappa B in infected HPMECs (miR-155 mimic vs . negative control, P = 0.004), and down-regulation of miR-155 had the opposite effect. In addition, S1PR1 was a direct target of miR-155 in the HPMECs. Inhibition of miR-155 enhanced the expression of the S1PR1 protein. Down-regulation of S1PR1 decreased the inhibitory effect of the miR-155 blockade on H1N1-induced cytokine production and nuclear factor kappa B activation in HPMECs. Conclusion: MiR-155 maybe modulate influenza A-induced inflammatory response by targeting S1PR1.

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Genes, environment, and developmental timing: New insights from translational approaches to understand early origins of respiratory diseases

Gutiérrez

Pérez

Rodríguez‐Martínez

et al. 2021

Pediatric Pulmonology

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Over the past decade, “omics” approaches have advanced our understanding of the molecular programming of the airways in humans. Several studies have identified potential molecular mechanisms that contribute to early life epigenetic reprogramming, including DNA methylation, histone modifications, microRNAs, and the homeostasis of the respiratory mucosa (epithelial function and microbiota). Current evidence supports the notion that early infancy is characterized by heightened susceptibility to airway genetic reprogramming in response to the first exposures in life, some of which can have life‐long consequences. Here, we summarize and analyze the latest insights from studies that support a novel epigenetic paradigm centered on human maturational and developmental programs including three cardinal elements: genes, environment, and developmental timing. The combination of these factors is likely responsible for the functional trajectory of the respiratory system at the molecular, functional, and clinical levels.

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The role of miR-155 in cigarette smoke-induced pulmonary inflammation and COPD

Cited by 59 publications

References 51 publications

Airway mir-155 responses are associated with TH1 cytokine polarization in young children with viral respiratory infections

Airway mir-155 responses are associated with TH1 cytokine polarization in young children with viral respiratory infections

Down-regulation of miR-155 inhibits inflammatory response in human pulmonary microvascular endothelial cells infected with influenza A virus by targeting sphingosine-1-phosphate receptor 1

Genes, environment, and developmental timing: New insights from translational approaches to understand early origins of respiratory diseases

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