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      The role of respiratory epithelium in host defence against influenza virus infection ☆

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      Author(s): , ∗
      Publication date (Electronic):
      Journal: Biomedical Journal
      Publisher: Chang Gung University
      Keywords: Influenza, Airway epithelium, Defence, Sensing, Injury and repair

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          Abstract

          The respiratory epithelium is the major interface between the environment and the host. Sophisticated barrier, sensing, anti-microbial and immune regulatory mechanisms have evolved to help maintain homeostasis and to defend the lung against foreign substances and pathogens. During influenza virus infection, these specialised structural cells and populations of resident immune cells come together to mount the first response to the virus, one which would play a significant role in the immediate and long term outcome of the infection. In this review, we focus on the immune defence machinery of the respiratory epithelium and briefly explore how it repairs and regenerates after infection.

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          Innate antiviral responses by means of TLR7-mediated recognition of single-stranded RNA.

          Sandra S. Diebold, Tsuneyasu Kaisho, Hiroaki Hemmi … (2004)
          Interferons (IFNs) are critical for protection from viral infection, but the pathways linking virus recognition to IFN induction remain poorly understood. Plasmacytoid dendritic cells produce vast amounts of IFN-alpha in response to the wild-type influenza virus. Here, we show that this requires endosomal recognition of influenza genomic RNA and signaling by means of Toll-like receptor 7 (TLR7) and MyD88. Single-stranded RNA (ssRNA) molecules of nonviral origin also induce TLR7-dependent production of inflammatory cytokines. These results identify ssRNA as a ligand for TLR7 and suggest that cells of the innate immune system sense endosomal ssRNA to detect infection by RNA viruses.
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            Alveolar macrophages: plasticity in a tissue-specific context.

            Tracy Hussell, Thomas Bell (2014)
            Alveolar macrophages exist in a unique microenvironment and, despite historical evidence showing that they are in close contact with the respiratory epithelium, have until recently been investigated in isolation. The microenvironment of the airway lumen has a considerable influence on many aspects of alveolar macrophage phenotype, function and turnover. As the lungs adapt to environmental challenges, so too do alveolar macrophages adapt to accommodate the ever-changing needs of the tissue. In this Review, we discuss the unique characteristics of alveolar macrophages, the mechanisms that drive their adaptation and the direct and indirect influences of epithelial cells on them. We also highlight how airway luminal macrophages function as sentinels of a healthy state and how they do not respond in a pro-inflammatory manner to antigens that do not disrupt lung structure. The unique tissue location and function of alveolar macrophages distinguish them from other macrophage populations and suggest that it is important to classify macrophages according to the site that they occupy.
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              Avian flu: influenza virus receptors in the human airway.

              Kyoko Shinya, Masahito Ebina, Shinya Yamada … (2006)
              Although more than 100 people have been infected by H5N1 influenza A viruses, human-to-human transmission is rare. What are the molecular barriers limiting human-to-human transmission? Here we demonstrate an anatomical difference in the distribution in the human airway of the different binding molecules preferred by the avian and human influenza viruses. The respective molecules are sialic acid linked to galactose by an alpha-2,3 linkage (SAalpha2,3Gal) and by an alpha-2,6 linkage (SAalpha2,6Gal). Our findings may provide a rational explanation for why H5N1 viruses at present rarely infect and spread between humans although they can replicate efficiently in the lungs.
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                Author and article information

                Contributors
                Ling-Pei Ho
                Journal
                Journal ID (nlm-ta): Biomed J
                Journal ID (iso-abbrev): Biomed J
                Title: Biomedical Journal
                Publisher: Chang Gung University
                ISSN (Print): 2319-4170
                ISSN (Electronic): 2320-2890
                Publication date PMC-release: 10 September 2018
                Publication date (Print): August 2018
                Publication date (Electronic): 10 September 2018
                Volume: 41
                Issue: 4
                Pages: 218-233
                Affiliations
                [1]MRC Human Immunology Unit, MRC Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford, UK
                Author notes
                [∗ ]Corresponding author. MRC Human Immunology Unit, University of Oxford, Oxford OX3 9DS, UK. ling-pei.ho@ 123456imm.ox.ac.uk
                Article
                Publisher ID: S2319-4170(18)30259-2
                DOI: 10.1016/j.bj.2018.08.004
                PMC ID: 6197993
                PubMed ID: 30348265
                SO-VID: 5caaa59e-10c1-463c-adcf-61775fc0252e
                Copyright © © 2018 Chang Gung University. Publishing services by Elsevier B.V.
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 6 June 2018
                Date accepted : 3 August 2018
                Categories
                Subject: Special Edition

                Keywords: influenza,airway epithelium,defence,sensing,injury and repair
                Data availability:
                Keywords: influenza, airway epithelium, defence, sensing, injury and repair

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