Pepsin as a causal agent of inflammation during nonacidic reflux
This article was presented at the Annual Meeting of the American Academy of Otolaryngology–Head and Neck Surgery, San Diego, CA, October 4-7, 2009.
Received 23 June 2009; received in revised form 13 August 2009; accepted 20 August 2009.
Refers to article:
Unexpected consequences of proton pump inhibitor use
Kenneth W. Altman, James A. Radosevich
Otolaryngology - Head and Neck Surgery
November 2009 (Vol. 141, Issue 5, Pages 564-566) Abstract |
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Abstract
Objective
To investigate the contribution of pepsin to inflammation attributed to nonacidic gastric reflux via analysis of inflammatory cytokine and cytokine receptor gene expression in pepsin-treated human hypopharyngeal epithelial cells in vitro.
Study Design
Translational research.
Setting
This study was performed in an academic research laboratory.
Subjects and Methods
Human hypopharyngeal epithelial cells were incubated with or without pepsin (0.1 mg/mL) at pH 7.4, 37°C, overnight. Expression of 84 inflammatory cytokines and cytokine receptors was analyzed via RT2 qPCR array.
Results
Expression of a number of inflammatory cytokines and receptors was altered in human hypopharyngeal epithelial cells following overnight treatment with pepsin at neutral pH. Greater than 1.5-fold change in gene expression was detected for CCL20, CCL26, IL8, IL1F10, IL1A, IL5, BCL6, CCR6, and CXCL14 (P < 0.05).
Conclusion
Exposure of hypopharyngeal cells to pepsin in a nonacidic environment induces the expression of several pro-inflammatory cytokines and receptors, including those known to be involved in inflammation of esophageal epithelium in response to reflux and which contribute to the pathophysiology of reflux esophagitis. These data indicate that refluxed pepsin may contribute to laryngeal inflammation associated with nonacidic gastric reflux, including that experienced by patients despite maximal acid suppression therapy.
Department of Otolaryngology and Communication Sciences, Medical College of Wisconsin, Milwaukee, WI
Corresponding author: Nikki Johnston, Department of Otolaryngology and Communication Sciences, Medical College of Wisconsin, 9200 W Wisconsin Avenue, Milwaukee, WI 53226
Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.
ABSTRACT