Host Protective Immune Responses against Influenza A Virus Infection

Jung, Hi Eun; Lee, Kyung-Mi

doi:10.3390/v12050504

Cited by 34 publications

(40 citation statements)

References 185 publications

(223 reference statements)

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“…The body's natural defense mechanism of inflammation which promotes cell repair and healing [107] was mimicked in our wdNHBE model, with the increased expression of proinflammatory cytokines and chemokines such as TNF, IL1B, IL6, CXCL8 and CXCL10. This suggests that wdNHBE cells recognize IAV and poly(I:C) through binding to pattern recognition receptors (PRRs) such as the Toll-like receptors (TLR3, TLR7, and TLR8), retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated protein-5 (MDA-5), triggering innate immune response signaling cascades as occurs in vivo [22,54,55,[108][109][110][111][112][113][114]. Antiviral, pro-and anti-inflammatory cytokines and chemokines are then upregulated in the host [27,56,115].…”

Section: Discussionmentioning

confidence: 99%

“…They form AJCs, exhibit ion transport, mucus secretion and mucociliary clearance [ 25 , 48 , 49 , 50 , 51 ]. wdNHBE cells also produce host–pathogen responses when exposed to respiratory viruses, such as the production of antiviral, immune and pro- and anti-inflammatory molecules [ 52 , 53 ], as occurs in the host in vivo (reviewed in: [ 20 , 21 , 22 , 27 , 54 , 55 , 56 , 57 ]). The response of airway epithelial cells (from different donors, cell preparations, etc.)…”

Section: Introductionmentioning

confidence: 99%

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Host–Pathogen Responses to Pandemic Influenza H1N1pdm09 in a Human Respiratory Airway Model

Pharo

Williams

Boyd

et al. 2020

Viruses

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The respiratory Influenza A Viruses (IAVs) and emerging zoonotic viruses such as Severe Acute Respiratory Syndrome-Coronavirus-2 (SARS-CoV-2) pose a significant threat to human health. To accelerate our understanding of the host–pathogen response to respiratory viruses, the use of more complex in vitro systems such as normal human bronchial epithelial (NHBE) cell culture models has gained prominence as an alternative to animal models. NHBE cells were differentiated under air-liquid interface (ALI) conditions to form an in vitro pseudostratified epithelium. The responses of well-differentiated (wd) NHBE cells were examined following infection with the 2009 pandemic Influenza A/H1N1pdm09 strain or following challenge with the dsRNA mimic, poly(I:C). At 30 h postinfection with H1N1pdm09, the integrity of the airway epithelium was severely impaired and apical junction complex damage was exhibited by the disassembly of zona occludens-1 (ZO-1) from the cell cytoskeleton. wdNHBE cells produced an innate immune response to IAV-infection with increased transcription of pro- and anti-inflammatory cytokines and chemokines and the antiviral viperin but reduced expression of the mucin-encoding MUC5B, which may impair mucociliary clearance. Poly(I:C) produced similar responses to IAV, with the exception of MUC5B expression which was more than 3-fold higher than for control cells. This study demonstrates that wdNHBE cells are an appropriate ex-vivo model system to investigate the pathogenesis of respiratory viruses.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Host–Pathogen Responses to Pandemic Influenza H1N1pdm09 in a Human Respiratory Airway Model

Pharo

Williams

Boyd

et al. 2020

Viruses

View full text Add to dashboard Cite

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“…An influenza virus infection can cause severe manifestations, such as pneumonia and acute respiratory distress syndrome [ 83 , 84 ]. The immune response against influenza virus is initiated by the airways epithelial cells, which secrete pro-inflammatory molecules such as IFNα/β, IL-6, TNF-α CCL2, CCL3, CCL5, and CXCL8, allowing the recruitment of natural killer (NK) cells, monocytes, macrophages, dendritic cells (DCs), and neutrophils [ 85 , 86 , 87 , 88 , 89 ]. Upon influenza infection, activated CD4+ T cells polarized to both Th1 and Th2 phenotypes, but Th1 cells are associated with survival after the infection [ 88 ].…”

Section: Neuroinflammation Induced By Respiratory Virusesmentioning

confidence: 99%

Contribution of Pro-Inflammatory Molecules Induced by Respiratory Virus Infections to Neurological Disorders

2021

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Neurobehavioral alterations and cognitive impairment are common phenomena that represent neuropsychiatric disorders and can be triggered by an exacerbated immune response against pathogens, brain injury, or autoimmune diseases. Pro-inflammatory molecules, such as cytokines and chemokines, are produced in the brain by resident cells, mainly by microglia and astrocytes. Brain infiltrating immune cells constitutes another source of these molecules, contributing to an impaired neurological synapse function, affecting typical neurobehavioral and cognitive performance. Currently, there is increasing evidence supporting the notion that behavioral alterations and cognitive impairment can be associated with respiratory viral infections, such as human respiratory syncytial virus, influenza, and SARS-COV-2, which are responsible for endemic, epidemic, or pandemic outbreak mainly in the winter season. This article will review the brain′s pro-inflammatory response due to infection by three highly contagious respiratory viruses that are the leading cause of acute respiratory illness, morbidity, and mobility in infants, immunocompromised and elderly population. How these respiratory viral pathogens induce increased secretion of pro-inflammatory molecules and their relationship with the alterations at a behavioral and cognitive level will be discussed.

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“…Activation and recruitment of these cells is often regulated by pattern recognition receptor (PRR) signaling (10,11). These pathogen sensing molecules promote the activation of multiple immune cell types and as such can be critical regulators of the early immune response to influenza virus infection (12).…”

Section: The Infant Immune Systemmentioning

confidence: 99%

Challenges for the Newborn Following Influenza Virus Infection and Prospects for an Effective Vaccine

Alexander-Miller

2020

Front. Immunol.

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Newborns are at significantly increased risk of severe disease following infection with influenza virus. This is the collective result of their naïve status, altered immune responsiveness, and the lack of a vaccine that is effective in these individuals. Numerous studies have revealed impairments in both the innate and adaptive arms of the immune system of newborns. The consequence of these alterations is a quantitative and qualitative decrease in both antibody and T cell responses. This review summarizes the hurdles newborns experience in mounting an effective response that can clear influenza virus and limit disease following infection. In addition, the challenges, as well as the opportunities, for developing vaccines that can elicit protective responses in these at risk individuals are discussed.

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Host Protective Immune Responses against Influenza A Virus Infection

Cited by 34 publications

References 185 publications

Host–Pathogen Responses to Pandemic Influenza H1N1pdm09 in a Human Respiratory Airway Model

Host–Pathogen Responses to Pandemic Influenza H1N1pdm09 in a Human Respiratory Airway Model

Contribution of Pro-Inflammatory Molecules Induced by Respiratory Virus Infections to Neurological Disorders

Challenges for the Newborn Following Influenza Virus Infection and Prospects for an Effective Vaccine

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