Evidence map›Paper›PMID 33868294›Full record

ReviewFrontiers in immunology2021

Influence of Hypoxia on the Epithelial-Pathogen Interactions in the Lung: Implications for Respiratory Disease.

Lee K Page, Karl J Staples, C Mirella Spalluto, Alastair Watson, Tom M A Wilkinson

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
5.9field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 52 citations in OpenAlex.

  1. Trial
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  7. The role and mechanisms of the HIF-1 signaling pathway in LC-COPD.Journal of cancer research and clinical oncology · 2025
    Review
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  9. Phase variation inMicrobiology spectrum · 2025
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 4 institutions in 1 country.

Lee K PageClinical and Experimental Sciences, University of Southampton Faculty of Medicine, Southampton, United Kingdom.
Karl J StaplesClinical and Experimental Sciences, University of Southampton Faculty of Medicine, Southampton, United Kingdom.
C Mirella SpallutoClinical and Experimental Sciences, University of Southampton Faculty of Medicine, Southampton, United Kingdom.
Alastair WatsonClinical and Experimental Sciences, University of Southampton Faculty of Medicine, Southampton, United Kingdom.
Tom M A WilkinsonClinical and Experimental Sciences, University of Southampton Faculty of Medicine, Southampton, United Kingdom.
Southampton General Hospital · GBNIHR Southampton Biomedical Research Centre · GBUniversity of Birmingham · GBUniversity of Southampton · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Under normal physiological conditions, the lung remains an oxygen rich environment. However, prominent regions of hypoxia are a common feature of infected and inflamed tissues and many chronic inflammatory respiratory diseases are associated with mucosal and systemic hypoxia. The airway epithelium represents a key interface with the external environment and is the first line of defense against potentially harmful agents including respiratory pathogens. The protective arsenal of the airway epithelium is provided in the form of physical barriers, and the production of an array of antimicrobial host defense molecules, proinflammatory cytokines and chemokines, in response to activation by receptors. Dysregulation of the airway epithelial innate immune response is associated with a compromised immunity and chronic inflammation of the lung. An increasing body of evidence indicates a distinct role for hypoxia in the dysfunction of the airway epithelium and in the responses of both innate immunity and of respiratory pathogens. Here we review the current evidence around the role of tissue hypoxia in modulating the host-pathogen interaction at the airway epithelium. Furthermore, we highlight the work needed to delineate the role of tissue hypoxia in the pathophysiology of chronic inflammatory lung diseases such as asthma, cystic fibrosis, and chronic obstructive pulmonary disease in addition to novel respiratory diseases such as COVID-19. Elucidating the molecular mechanisms underlying the epithelial-pathogen interactions in the setting of hypoxia will enable better understanding of persistent infections and complex disease processes in chronic inflammatory lung diseases and may aid the identification of novel therapeutic targets and strategies.

Indexed as

COVID-19Host-Pathogen InteractionsHumansHypoxiaLungRespiratory MucosaSARS-CoV-2epithelial cellshost-pathogen interactionshypoxiahypoxia-inducible factor (HIF)-1innate immunityrespiratory disease

Identifiers

PMID33868294
PMCPMC8044850
OpenAlexW3137034646

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.