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International Journal of Inflammation
Volume 2011 (2011), Article ID 569416, 5 pages
http://dx.doi.org/10.4061/2011/569416
Research Article

Cytotoxicity and Induction of Inflammation by Pepsin in Acid in Bronchial Epithelial Cells

1ELEGI, Colt Research Laboratories, MRC Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, Edinburgh EH 16 4TJ, UK
2Department of Medical Microbiology, University Medical Center Utrecht, 3508 Utrecht, The Netherlands

Received 23 February 2011; Revised 17 May 2011; Accepted 20 May 2011

Academic Editor: Jean-Marc Cavaillon

Copyright © 2011 Erik Bathoorn et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Introduction. Gastroesophageal reflux has been associated with chronic inflammatory diseases and may be a cause of airway remodelling. Aspiration of gastric fluids may cause damage to airway epithelial cells, not only because acidity is toxic to bronchial epithelial cells, but also since it contains digestive enzymes, such as pepsin. Aim. To study whether pepsin enhances cytotoxicity and inflammation in airway epithelial cells, and whether this is pH-dependent. Methods. Human bronchial epithelial cells were exposed to increasing pepsin concentrations in varying acidic milieus, and cell proliferation and cytokine release were assessed. Results. Cell survival was decreased by pepsin exposure depending on its concentration ( 𝐹 = 1 7 . 4 ) and pH level of the medium ( 𝐹 = 6 . 5 ) (both 𝑃 < 0 . 0 1 ). Pepsin-induced interleukin-8 release was greater at lower pH ( 𝐹 = 5 . 1 ; 𝑃 < 0 . 0 1 ). Interleukin-6 induction by pepsin was greater at pH 1.5 compared to pH 2.5 (mean difference 434%; 𝑃 = 0 . 0 3 ). Conclusion. Pepsin is cytotoxic to bronchial epithelial cells and induces inflammation in addition to acid alone, dependent on the level of acidity. Future studies should assess whether chronic aspiration causes airway remodelling in chronic inflammatory lung diseases.