Original contribution
Assessment of desmosomal components
(desmoglein 1-3, plakoglobin) in cardia mucosa
in relation to gastroesophageal reflux disease and
Helicobacter pylori infection
☆
Thomas Wex PhD
a,
⁎
,1
, Doerthe Kuester MD
b,1
, Klaus Mönkemüller MD
a,2
,
Antje Stahr MD
a
, Lucia C. Fry MD
a,2
, Arne Kandulski MD
a
, Siegfried Kropf PhD
c
,
Albert Roessner MD
b
, Peter Malfertheiner MD
a
a
Department of Gastroenterology, Hepatology and Infectious Diseases, Otto-von-Guericke University,
39120 Magdeburg, Germany
b
Institute of Pathology, Otto-von-Guericke University Magdeburg, D-39120 Magdeburg, Germany
c
Institute of Biometrics and Medical Informatics, Otto-von-Guericke University Magdeburg, D-39120 Magdeburg, Germany
Received 9 August 2011; revised 2 December 2011; accepted 8 December 2011
Keywords:
Cardia mucosa;
Desmoglein;
Desmosomes;
Gastroesophageal reflux
diseases;
GERD;
H pylori
Summary Gastroesophageal reflux disease is associated with impaired epithelial barrier function and
abnormal expression of proteins forming cell-cell contacts by tight junctions and desmosomes in distal
esophageal squamous mucosa. Although gastroesophageal reflux disease and Helicobacter pylori are
both associated with chronic inflammation of the adjacent cardia mucosa, it is not known whether these
lead to derangements of the desmosomal complexes. Here, we assessed the expression of 4 proteins
(plakoglobin and desmoglein 1, 2, and 3) forming epithelial desmosomal complexes by quantitative
reverse transcription polymerase chain reaction and immunohistochemistry in biopsies from 67 patients
with gastroesophageal reflux disease and 23 gastroesophageal reflux disease–negative controls.
Plakoglobin and desmoglein 2 were ubiquitously expressed in all samples, whereas desmoglein 1 and 3
were not expressed in cardia mucosa. Gastroesophageal reflux disease was specifically associated with
elevated transcript levels of desmoglein 2 and plakoglobin. These were significantly increased from 2.0-
to 2.7-fold in patients with gastroesophageal reflux disease compared with controls (P b .01), and
significantly increased immunohistochemical scores for both proteins were observed (P b .05) as well.
The combined presence of gastroesophageal reflux disease and Helicobacter pylori infection had no
additional effect on desmosomal gene expression. Taken together, the up-regulation of plakoglobin and
desmoglein 2 in cardia mucosa of patients with gastroesophageal reflux disease supports the concept that
the “transition zone” between distal esophagus and proximal stomach is affected by gastroesophageal
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☆
Disclosure/Conflict of Interest: The authors declare that none of them has financial interests in context to this study. This work was partially supported by
the NBL-3 program of the “Bundesministerium für Forschung und Technik” (01ZZ0407/PFG1). T.W. was supported by the Deutsche Forschungsgemeinschaft
(WE2170/8-1).
⁎
Corresponding author. Department of Gastroenterology, Hepatology and Infectious Diseases, Otto-von-Guericke University, Magdeburg, 39120
Magdeburg, Germany.
E-mail address: thomas.wex@med.ovgu.de (T. Wex).
1
Contributed equally to the study.
2
Current address: Department of Gastroenterology, Hepatology, and Infectious Diseases, Marienhospital, 46236 Bottrop, Germany.
0046-8177/$ – see front matter © 2012 Elsevier Inc. All rights reserved.
doi:10.1016/j.humpath.2011.12.024
Human Pathology (2012) 43, 1745–1754