Gastroesophageal reflux disease leads to major alterations in lectin-binding in the columnar epithelium of the gastroesophageal junction.
OBJECTIVE
Chronic gastritis and esophagitis are associated with changes in glycosylation patterns. Lectins are carbohydrate-binding proteins that are used as sensitive tools in the analysis of glycosylation patterns. The aim was to investigate the binding patterns of lectins UEA-I, DBA, HPA and PNA at the squamocolumnar junction in relation to the existence of gastroesophageal reflux disease (GERD) and Helicobacter pylori (H. pylori) infection.


METHODS
Eighty-eight patients with either dyspeptic or gastroesophageal reflux-related symptoms were included in the study and stratified into four subgroups based on the presence of GERD and H. pylori infection. The binding patterns of lectins were examined immunohistochemically at the squamocolumnar junction, in squamous (SE) and columnar-lined epithelium (CLE). Staining patterns of lectins were semiquantitatively evaluated using an immunohistochemical score; data were analyzed using the non-parametric Mann-Whitney U-test.


RESULTS
The presence of GERD led to significant changes in lectin-binding patterns. Lectin-binding was significantly reduced for UEA-I (p<0.0001), DBA (p<0.0001), PNA (p<0.01) and DBA (p<0.05) in CLE and SE of patients with GERD, respectively. H. pylori infection was associated with reduced PNA and DBA binding to the deep glandular mucosa of CLE (p<0.05) and surface SE (p<0.05), respectively.


CONCLUSIONS
Distinct and complex changes in lectin-staining patterns are most prominent in CLE of patients with GERD. The functional relevance of changes in the glycosylation patterns needs further investigation.
Neumann
Helmut
H
Otto-von-Guericke University Magdeburg, Department of Gastroenterology, Hepatology and Infectious Diseases, Magdeburg, Germany.
Wex
Thomas
T
Vieth
Michael
M
Peitz
Ulrich
U
Roessner
Albert
A
Malfertheiner
Peter
P
D001706:Biopsy; D016099:Endoscopy, Gastrointestinal; D004943:Esophagogastric Junction / Q000378:metabolism* / Q000473:pathology; D005753:Gastric Mucosa / Q000378:metabolism* / Q000473:pathology; D005756:Gastritis / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D005764:Gastroesophageal Reflux / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D006031:Glycosylation; D016481:Helicobacter Infections / Q000378:metabolism*; D016480:Helicobacter pylori / Q000302:isolation & purification; D006801:Humans; D007150:Immunohistochemistry; D037102:Lectins / Q000378:metabolism*; D018709:Statistics, Nonparametric
D037102:Lectins