From gastric aspiration to airway inflammation

https://doi.org/10.4081/monaldi.2010.299

Authors

  • I.A. Brownlee | j.p.pearson@ncl.ac.uk Institute for Cell & Molecular Biosciences, Medical School, Newcastle University, Newcastle-upon Tyne, NE2 4HH, United Kingdom.
  • A. Aseeri Institute for Cell & Molecular Biosciences, Medical School, Newcastle University, Newcastle-upon Tyne, NE2 4HH, United Kingdom.
  • C. Ward Institute of Cellular Medicine, Medical School, Newcastle University, Newcastle-upon Tyne, NE2 4HH, United Kingdom.
  • J.P. Pearson Institute for Cell & Molecular Biosciences, Medical School, Newcastle University, Newcastle-upon Tyne, NE2 4HH, United Kingdom.

Abstract

The airways are poorly protected from potentially damaging agents contained within gastric contents. While digestive factors are obvious damaging agents, gastric aspiration may also deliver microbial agents, cytokines or food antigens to airway tissues. Direct damage or the triggering of the inflammatory cascade by gastric aspiration is believed to drive airways disease onset and/or progression. Evidence exists from experimental models demonstrating direct instillation of damaging factors to a range of airways epithelia causes damage and/or an inflammatory response. Clinical longitudinal studies have also noted an association between the presence of biomarkers of reflux in airways samples and disease progression. A shared pathophysiology of many chronic airways diseases is a more negative intrathoracic pressure. Such changes would drive an increased abdominothoracic pressure gradient. These changes in respiratory mechanics mean that chronic lung disease patients may be predisposed to reflux and subsequent aspiration. Therefore, it appears that gastric aspiration and airways disease progression may be linked not solely as cause and effect, but seemingly within a vicious cycle. A range of physiological factors govern both occurrence of gastric reflux into the pharynx/larynx and could also increase the susceptibility of certain individuals to disease progression. A range of long-term surgical and pharmacological intervention studies are necessary to test the benefit of such therapies in reducing disease progression or driving symptom improvement. Such studies may be hampered by the reliability of available therapies in halting gastric aspiration and the difficulty in the clinical or biochemical assessment of gastric aspiration.

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Published
2016-01-19
Info
Issue
Section
Editorial
Keywords:
Pepsin, Aspiration, Reflux, Epithelial mesenchymal transition, Inflammation, Bile salts
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  • PDF: 379
How to Cite
Brownlee, I.A., A. Aseeri, C. Ward, and J.P. Pearson. 2016. “From Gastric Aspiration to Airway Inflammation”. Monaldi Archives for Chest Disease 73 (2). https://doi.org/10.4081/monaldi.2010.299.