Human nasal epithelial cells derived from multiple subjects exhibit differential responses to H3N2 influenza virus infection in vitro

Yan, Yan; Tan, Kai Sen; Li, Chunwei; Tran, Thai; Chao, Siew Shuen; Sugrue, Richard J.; Li, Shi; Chow, Vincent T. K.; Wang, Deyun

doi:10.1016/j.jaci.2015.11.016

Cited by 44 publications

(68 citation statements)

References 34 publications

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“…The human airway epithelial cells are the main target as well as primary contact site of IAV with the host, and these cells respond to IAV infection via expressing several inflammatory genes and immune responses that protect cells against viral infection . So far, several in vivo and in vitro studies have indicated that miRNAs have a differing role in the regulation of innate immune system responses to influenza virus infection, but have still to focus on primary contact site of the viral infections, the nasal epithelium . miR‐146a‐5p, through gene expression regulation in monocytes and macrophages, is known as a significant determinant of the host innate and adaptive immune responses .…”

Section: Mir‐146a In Influenzamentioning

confidence: 99%

The role of miR‐146a in viral infection

et al. 2019

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Cellular microRNAs (miRNAs) were identified as a key player in the posttranscriptional regulation of cellular‐genes regulatory pathways. They also emerged as a significant regulator of the immune response. In particular, miR‐146a acts as an importance modulator of function and differentiation cells of the innate and adaptive immunity. It has been associated with disorder including cancer and viral infections. Given its significance in the regulation of key cellular processes, it is not surprising which virus infection have found ways to dysregulation of miRNAs. miR‐146a has been identified in exosomes (exosomal miR‐146a). After the exosomes release from donor cells, they are taken up by the recipient cell and probably the exosomal miR‐146a is able to modulate the antiviral response in the recipient cell and result in making them more susceptible to virus infection. In this review, we discuss recent reports regarding miR‐146a expression levels, target genes, function, and contributing role in the pathogenesis of the viral infection and provide a clue to develop the new therapeutic and preventive strategies for viral disease in the future.

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Section: Mir‐146a In Influenzamentioning

confidence: 99%

The role of miR‐146a in viral infection

et al. 2019

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“…Dissociated cells were fixed in 4% formaldehyde at room temperature for 10 min, followed by washing with 1× Dulbecco’s phosphate-buffered saline and centrifugation. Cytospin (1–2 ×10 4 cells/slide) preparations were prepared at 500 rpm for 5 min using a Shandon Cytospin 3 Cytocentrifuge (Thermo Fisher Scientific) [16]. …”

Section: Methodsmentioning

confidence: 99%

Downregulation and Aberrant Localization of Forkhead Box J1 in Allergic Nasal Mucosa

Peng

Chen

Guan

et al. 2018

Int Arch Allergy Immunol

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Background: Forkhead box J1 (FOXJ1) plays pivotal roles in motile cilia formation. However, it remains unclear whether abnormal expression or localization of FOXJ1 in nasal mucosa tissues is associated with allergic rhinitis (AR), in which impaired mucociliary clearance is implicated. Objective: We sought to investigate the expression and localization of FOXJ1 in inferior turbinate from patients with AR and controls. Methods: We assayed mRNA levels of FOXJ1, DNAI1, DNALI1, and DNAH9 by using whole-genome expression array and quantitative real-time polymerase chain reaction. We elucidated the localization of FOXJ1 by using immunofluorescence assays in paraffin sections and primary single cells. Four patterns of FOXJ1 localization (normal, N; intermediate, I; mislocalization, M; absence, A) were defined. We developed a semiquantitative scoring system to elucidate their localization in 5 areas per paraffin section, with individual sections being assigned a score between 0 and 2. Results: The mRNA levels of FOXJ1, DNAI1, DNALI1, and DNAH9 were significantly reduced in patients with AR compared with controls (all p < 0.05). The median (1st and 3rd quartile) of the FOXJ1 score was 0.4 (0.0 and 0.85) in patients with AR, and 0.2 (0.0 and 0.4) in controls (p < 0.05). For primary cytospin samples, the mean percentages of FOXJ1 localization patterns N, I, M, and A were 46.7, 10.0, 30.0, and 26.7% in patients with AR, and 82.5, 5.0, 5.0, and 7.5% in controls, respectively (p < 0.05). Conclusion: Downregulation and aberrant localization of FOXJ1 may be crucial characteristics of the allergic nasal mucosa.

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“…In the case of COPD, increased ILC2 activation, which retain the capability of differentiating to ILC1, may also further augment the neutrophilic response and further aggravate the exacerbation (Silver et al, 2016). Interestingly, these factors are not released to any great extent and do not activate an ILC2 response during viral infection in healthy individuals (Yan et al, 2016;Tan et al, 2018a); despite augmenting a type 2 exacerbation in chronically inflamed airways (Jurak et al, 2018). These classical mechanisms of viral induced acute exacerbations are summarized in Figure 1.…”

Section: Current Understanding Of Viral Induced Exacerbation Of Chronmentioning

confidence: 99%

“…On the other end of the spectrum, viruses that induce strong type 1 inflammation and cell death such as IFV (Yan et al, 2016;Guibas et al, 2018) and certain CoV (including the recently emerged COVID-19 virus) (Tao et al, 2013;Yue et al, 2018;Zhu et al, 2020), may not cause prolonged inflammation due to strong induction of antiviral clearance. These infections, however, cause massive damage and cell death to the epithelial barrier, so much so that areas of the epithelium may be completely absent post infection (Yan et al, 2016;Tan et al, 2019). Factors such as RANTES and CXCL10, which recruit immune cells to induce apoptosis, are strongly induced from IFV infected epithelium (Ampomah et al, 2018;Tan et al, 2019).…”

Section: Destruction Of the Epithelial Barriermentioning

confidence: 99%

Respiratory Viral Infections in Exacerbation of Chronic Airway Inflammatory Diseases: Novel Mechanisms and Insights From the Upper Airway Epithelium

Tan

Lim

Liu

et al. 2020

Front. Cell Dev. Biol.

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Respiratory virus infection is one of the major sources of exacerbation of chronic airway inflammatory diseases. These exacerbations are associated with high morbidity and even mortality worldwide. The current understanding on viral-induced exacerbations is that viral infection increases airway inflammation which aggravates disease symptoms. Recent advances in in vitro air-liquid interface 3D cultures, organoid cultures and the use of novel human and animal challenge models have evoked new understandings as to the mechanisms of viral exacerbations. In this review, we will focus on recent novel findings that elucidate how respiratory viral infections alter the epithelial barrier in the airways, the upper airway microbial environment, epigenetic modifications including miRNA modulation, and other changes in immune responses throughout the upper and lower airways. First, we reviewed the prevalence of different respiratory viral infections in causing exacerbations in chronic airway inflammatory diseases. Subsequently we also summarized how recent models have expanded our appreciation of the mechanisms of viral-induced exacerbations. Further we highlighted the importance of the virome within the airway microbiome environment and its impact on subsequent bacterial infection. This review consolidates the understanding of viral induced exacerbation in chronic airway inflammatory diseases and indicates pathways that may be targeted for more effective management of chronic inflammatory diseases.

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Human nasal epithelial cells derived from multiple subjects exhibit differential responses to H3N2 influenza virus infection in vitro

Cited by 44 publications

References 34 publications

The role of miR‐146a in viral infection

The role of miR‐146a in viral infection

Downregulation and Aberrant Localization of Forkhead Box J1 in Allergic Nasal Mucosa

Respiratory Viral Infections in Exacerbation of Chronic Airway Inflammatory Diseases: Novel Mechanisms and Insights From the Upper Airway Epithelium

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