Host defense function of the airway epithelium in health and disease: clinical background
Open accessAbstract
Respiratory infection is extremely common and a major cause of morbidity and mortality worldwide. The airway epithelium has an important role in host defense against infection and this is illustrated in this review by considering infection by respiratory viruses. In patients with asthma or chronic obstructive pulmonary disease, respiratory viruses are a common trigger of exacerbations. Rhinoviruses (RV) are the most common virus type detected. Knowledge of the immunopathogenesis of such RV-induced exacerbations remains limited, but information is available from in vitro and from in vivo studies, especially of experimental infection in human volunteers. RV infects and replicates within epithelial cells (EC) of the lower respiratory tract. EC are an important component of the innate-immune response to RV infection. The interaction between virus and the intracellular signaling pathways of the host cell results in activation of potentially antiviral mechanisms, including type 1 interferons and nitric oxide, and in the producton of cytokines and chemokines [interleukin (IL)-1β, IL-6, IL-8, IL-11, IL-16, tumor necrosis factor α, granulocyte macrophage-colony stimulating factor, growth-regulated oncogene-α, epithelial neutrophil-activating protein-78, regulated on activation, normal T expressed and secreted, eotaxin 1/2, macrophage-inflammatory protein-1α], which influence the subsequent induced innate- and specific-immune response. Although this is beneficial in facilitating clearance of virus from the respiratory tract, the generation of proinflammatory mediators and the recruitment of inflammatory cells result in a degree of immunopathology and may amplify pre-existing airway inflammation. Further research will be necessary to determine whether modification of EC responses to respiratory virus infection will be of therapeutic benefit.
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Infection of human airway epithelial cells with respiratory viruses induces rapid cytokine and chemokine gene expression through activation of proinflammatory transcription factors including NF-kB, AP-1, and STAT1/2.
“Infection of human airway epithelial cells with respiratory viruses induces rapid cytokine and chemokine gene expression through activation of several proinflammatory transcription factors. These include NF-κB, AP-1, and STAT1/2 (123, 181).”
From The airway epithelium: soldier in the fight against respiratory viruses (2011) · cites this paper as [181]
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Guillot, L., Le Goffic, R., Bloch, S., Escriou, N., Akira, S., Chignard, M., & Si-Tahar, M. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m410592200 · Cited by 689 · see citing works
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- Authors
- Message, S. D., & Johnston, S. L.
- Affiliations
- Imperial College London (GB)
- Venue
- Journal of Leukocyte Biology
- Publisher
- Oxford University Press (OUP)
- Published
- 2003-09-12
- Volume
- 75
- Issue
- 1
- Pages
- 5-17
- ISSN
- 0741-5400 (ISSN-L)
- 1938-3673
- PMC
- PMC7167170
- OpenAlex
- W2084684444
- Cited by
- 159
- References
- 176
- Citations by year
- 2026: 1 · 2025: 6 · 2024: 2 · 2023: 3 · 2022: 1 · 2021: 6 · 2020: 7 · 2019: 2 · 2018: 2 · 2017: 2 · 2016: 6 · 2015: 11 · 2014: 9 · 2013: 4 · 2012: 2
- FWCI
- 1.37
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Leukocyte Biology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Medical Research Council
- British Lung Foundation Programme
- Topics
- Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
- Health Sciences › Medicine › Epidemiology › Respiratory viral infections research
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Keywords
- airway epithelium, host defense, respiratory viruses, rhinovirus, asthma exacerbations, COPD exacerbations, innate immunity, type I interferon, nitric oxide, cytokines and chemokines, immunopathogenesis, epithelial cells, airway inflammation
- MeSH terms
- Adult, Asthma, Child, Humans, Infant, Reference Values, Respiratory Tract Diseases, Virus Diseases, Cytokines, Chemokines, Respiratory Mucosa
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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