Lung epithelial cells resist influenza A infection by inducing the expression of cytochrome c oxidase VIc which is modulated by miRNA 4276

Othumpangat, Sreekumar; Noti, John D.; Beezhold, Donald H.

doi:10.1016/j.virol.2014.08.007

Cited by 42 publications

(38 citation statements)

References 34 publications

(41 reference statements)

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“…All primers and probes were custom synthesized by Life Technologies. To determine the relative matrix gene copy number from influenza virus strains, a standard curve was generated from the cloned influenza H1N1 matrix gene and analyzed concurrently with RT-PCR reactions (Othumpangat et al, 2014). …”

Section: Methodsmentioning

confidence: 99%

ICAM-1 regulates the survival of influenza virus in lung epithelial cells during the early stages of infection

et al. 2016

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Intercellular cell adhesion molecule-1 (ICAM-1) is an inducible cell surface glycoprotein that is expressed on many cell types. Influenza virus infection enhanced ICAM-1 expression and messenger RNA levels. Human bronchial epithelial cells (HBEpC) and nasal epithelial cells, on exposure to different strains of influenza virus (H1N1, H3N2, and H9N1) showed significant increase in ICAM-1 gene expression (p<0.001) along with the ICAM-1 protein levels (surface and secreted). Depleting ICAM-1 in HBEpC with ICAM-1 siRNA and subsequently infecting with H1N1 showed increased viral copy numbers. Influenza virus infection in HBEpC resulted in up-regulation of NF-κB protein and the lack of ICAM-1 decreased NF-κB activity in NF-κB luciferase reporter assay. Addition of exogenous IL-1β to HBEpC induced the ICAM-1 expression and decreased matrix gene copy number. Taken together, HBEpC induced ICAM-1 plays a key role in modulating the influenza virus survival possibly through the NF-κB pathway.

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Section: Methodsmentioning

confidence: 99%

ICAM-1 regulates the survival of influenza virus in lung epithelial cells during the early stages of infection

et al. 2016

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“…Immediately upon infection, it is beneficial for IAV to block epithelial cell apoptosis to avoid destroying its replicative niche and this is primarily mediated by viral NS1. Early blockage of apoptosis by IAV is counteracted by host mechanisms, such as IFN-I signaling, to induce apoptosis and resist viral replication [69]. Yet, following initial replication cycles, at later time points, IAV must activate apoptotic pathways to generate new infectious virions, promote budding at the cell surface and facilitate subsequent rounds of infection in neighboring cells.…”

Section: Apoptosis In Iav-infected Lung Epithelial Cellsmentioning

confidence: 99%

Dissecting host cell death programs in the pathogenesis of influenza

Downey

Pernet

François

et al. 2018

Microbes and Infection

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Influenza A virus (IAV) is a pulmonary pathogen, responsible for significant yearly morbidity and mortality. Due to the absence of highly effective antiviral therapies and vaccine, as well as the constant threat of an emerging pandemic strain, there is considerable need to better understand the host-pathogen interactions and the factors that dictate a protective versus detrimental immune response to IAV. Even though evidence of IAV-induced cell death in human pulmonary epithelial and immune cells has been observed for almost a century, very little is known about the consequences of cell death on viral pathogenesis. Recent study indicates that both the type of cell death program and its kinetics have major implications on host defense and survival. In this review, we discuss advances in our understanding of cell death programs during influenza virus infection, in hopes of fostering new areas of investigation for targeted clinical intervention.

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“…The lung is one of the organs most affected by acute HSV-1 infection. DCs, macrophages, and epithelial cells of the lung have been reported to play critical roles in viral infection (38,39). Therefore, we next examined these cellular populations, which might have been responsible for the increased resistance of Cav-1 Ϫ/Ϫ mice.…”

Section: Resultsmentioning

confidence: 99%

Herpes Simplex Virus 1 Suppresses the Function of Lung Dendritic Cells via Caveolin-1

Geng

et al. 2015

Clin Vaccine Immunol

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Caveolin-1 (Cav-1), the principal structural protein of caveolae, has been implicated as a regulator of virus-host interactions. Several viruses exploit caveolae to facilitate viral infections. However, the roles of Cav-1 in herpes simplex virus 1 (HSV-1) infection have not fully been elucidated. Here, we report that Cav-1 downregulates the expression of inducible nitric oxide synthase (iNOS) and the production of nitric oxide (NO) in dendritic cells (DCs) during HSV-1 infection. As a result, Cav-1 deficiency led to an accelerated elimination of virus and less lung pathological change following HSV-1 infection. This protection was dependent on iNOS and NO production in DCs. Adoptive transfer of DCs with Cav-1 knockdown was sufficient to confer the protection to wild-type (WT) mice. In addition, Cav-1 knockout (KO) (Cav-1 ؊/؊ ) mice treated with an iNOS inhibitor exhibited significantly reduced survival compared to that of the nontreated controls. We found that Cav-1 colocalized with iNOS and HSV-1 in caveolae in HSV-1-infected DCs, suggesting their interaction. Taken together, our results identified Cav-1 as a novel regulator utilized by HSV-1 to evade the host antiviral response mediated by NO production. Therefore, Cav-1 might be a valuable target for therapeutic approaches against herpesvirus infections. Herpes simplex virus 1 (HSV-1) is a double-stranded DNA (dsDNA) virus belonging to the Alphaherpesvirus family, which causes oral herpes, encephalitis, keratitis, neonatal herpes, and pneumonia disease, establishing latency in the neurons after acute infection of mucosal tissues (1-3). Notably, HSV-1 can be isolated from the respiratory tract of immunosuppressed patients and newborn infants, where it induces pneumonitis, resulting in remarkable morbidity and mortality (4). Recent studies have suggested that HSV-1-induced bronchopneumonitis is common in nonimmunocompromised persons who are undergoing continuous mechanical ventilation (5). Currently, the mechanisms of HSV-1-induced pneumonia and obstructive pulmonary disease are not fully understood, although intranasal (i.n.) infection with HSV-1 in mice can be used as a model to investigate these mechanisms (4, 6, 7). Such investigations might reveal a valuable therapeutic approach for HSV-1-induced pneumonia.Innate defense cells and inflammatory factors serve as the firstline of host defense against viral infections. DCs can be recruited to the lungs and in the cornea of the eye, where they contribute to host defense (8, 9). Studies have shown that diphtheria toxin (DT)-induced depletion of DCs in CD11c-DTR mice (in which the DT receptor [DTR] is expressed under the control of the CD11c promoter) inhibited the migration of natural killer cells and neutrophils to locally infected cornea, resulting in severe pathology (10, 11). Moreover, involvement of the free radical nitric oxide (NO) has been indicated. This is a powerful vasodilator factor and cell signaling molecule, with a short half-life of 3 to ϳ4 s in the blood, and it is synthesized by nitric oxide s...

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Lung epithelial cells resist influenza A infection by inducing the expression of cytochrome c oxidase VIc which is modulated by miRNA 4276

Cited by 42 publications

References 34 publications

ICAM-1 regulates the survival of influenza virus in lung epithelial cells during the early stages of infection

ICAM-1 regulates the survival of influenza virus in lung epithelial cells during the early stages of infection

Dissecting host cell death programs in the pathogenesis of influenza

Herpes Simplex Virus 1 Suppresses the Function of Lung Dendritic Cells via Caveolin-1

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