Dissecting host cell death programs in the pathogenesis of influenza

Downey, Jeffrey; Pernet, Erwan; François, Clément; Divangahi, Maziar

doi:10.1016/j.micinf.2018.03.005

Cited by 23 publications

(25 citation statements)

References 145 publications

(174 reference statements)

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“…As IAV can hijack a series of host cellular processes such as cell death machinery, the development of novel therapeutics targeting cell death during IAV infection has previously been suggested 111 . However, here we outlined and discussed the complexity of IAV-induced cell death.…”

Section: Discussionmentioning

confidence: 99%

The induction and consequences of Influenza A virus-induced cell death

et al. 2018

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Infection with Influenza A virus (IAV) causes significant cell death within the upper and lower respiratory tract and lung parenchyma. In severe infections, high levels of cell death can exacerbate inflammation and comprise the integrity of the epithelial cell barrier leading to respiratory failure. IAV infection of airway and alveolar epithelial cells promotes immune cell infiltration into the lung and therefore, immune cell types such as macrophages, monocytes and neutrophils are readily exposed to IAV and infection-induced death. Although the induction of cell death through apoptosis and necrosis following IAV infection is a well-known phenomenon, the molecular determinants responsible for inducing cell death is not fully understood. Here, we review the current understanding of IAV-induced cell death and critically evaluate the consequences of cell death in aiding either the restoration of lung homoeostasis or the progression of IAV-induced lung pathologies.

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Section: Discussionmentioning

confidence: 99%

The induction and consequences of Influenza A virus-induced cell death

et al. 2018

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“…Programmed cell death, especially necroptosis has emerged as an important mechanism in the pathogenesis of influenza (Atkin-Smith et al, 2018; Downey et al, 2018; Fujikura and Miyazaki, 2018). The central model of necroptosis involves RIPK3 and the RIPK3-mediated p-MLKL (Cho et al, 2009; He et al, 2009; Sun et al, 2012; Zhao et al, 2012; Wang et al, 2014; Silke et al, 2015; Wallach et al, 2016; He and Wang, 2018).…”

Section: Discussionmentioning

confidence: 99%

Influenza Virus Infection Induces ZBP1 Expression and Necroptosis in Mouse Lungs

Wang

Qin

Florence

et al. 2019

Front. Cell. Infect. Microbiol.

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Programmed cell death and especially necroptosis, a programmed and regulated form of necrosis, have been recently implicated in the progression and outcomes of influenza in mouse models. Moreover, Z-DNA/RNA binding protein 1 (ZBP1) has been identified as a key signaling molecule for necroptosis induced by Influenza A virus (IAV). Direct evidence of IAV-induced necroptosis has not been shown in infected lungs in vivo . It is also unclear as to what cell types undergo necroptosis during pulmonary IAV infection and whether ZBP1 expression can be regulated by inflammatory mediators. In this study, we found that IAV infection induced ZBP1 expression in mouse lungs. We identified that mediators implicated in the pathogenesis of IAV infection including interferons (IFNs), TNFα, and agonists for Toll-like receptors 3 and 4 were potent inducers of ZBP1 expression in primary murine alveolar epithelial cells, bone marrow derived macrophages, and dendritic cells. We further found that IAV infection induced a strong necroptosis through phosphorylation of the necroptosis effector mixed lineage kinase domain-like protein in infiltrating immune cells and alveolar epithelial cells by day 7 post-infection. Lastly, we found different cell type-specific responses to IAV-induced cell death upon inhibition of caspases and/or necroptosis pathways. Our findings provide direct evidence that IAV infection induces necroptosis in mouse lungs, which may involve local induction of ZBP1 and different programmed cell death signaling mechanisms in alveolar epithelial and infiltrating inflammatory cells in the lungs.

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“…And even when the complexity of the pathogen world is narrowed down to "only" the influenza A virus (IAV), things stay pretty convoluted, as Downey et al point out in their review. They emphasize the importance of using in vivo models rather than cell cultures because communication between pulmonary macrophages and epithelial cells shape the kinetics of cell death during infection, which are in turn crucial for regulating the antiviral responses [7]. This view is supported by Brizic et al, who describe insights on the neurological damage caused by the human cytomegalovirus (HCMV) gained from a mouse model [8].…”

Section: Times Of Technologymentioning

confidence: 99%

Microbes and Infection turns 20

Häfner

Ojcius

2018

Microbes and Infection

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The journal Microbes and Infection is celebrating its vigintennial anniversary and has reunited for this occasion two dozen reviews illustrating achievements of the past as well as future challenges in the field of infectious diseases. From top-notch vaccine development strategies, to high-throughput powered analysis of complex host-pathogen interactions, to innovative therapeutic designs, this issue covers the entire spectrum of pathogens and areas of their confrontation with the host.

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Dissecting host cell death programs in the pathogenesis of influenza

Cited by 23 publications

References 145 publications

The induction and consequences of Influenza A virus-induced cell death

The induction and consequences of Influenza A virus-induced cell death

Influenza Virus Infection Induces ZBP1 Expression and Necroptosis in Mouse Lungs

Microbes and Infection turns 20

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