Gastroesophageal reflux disease does not lead to changes in the secretory leukocyte protease inhibitor expression in esophageal mucosa.
OBJECTIVE
Secretory leukocyte protease inhibitor (SLPI) serves as a 'defense shield' against serine proteases in inflammation. Gastroesophageal reflux disease (GERD) is associated with chronic inflammation and histomorphological alterations of the gastroesophageal junction and esophageal mucosa. Here, it was investigated whether the presence of GERD was associated with changes of mucosal SLPI expression.


METHODS
Ninety-five patients with GERD-related symptoms and 27 patients lacking those symptoms were included. Endoscopic and histological evaluation was done according to the Los Angeles and updated Sydney classifications. Multiple biopsies were taken from gastric and esophageal mucosa of each patient for histology, immunohistochemistry (IHC), and molecular analyses. SLPI expression was analyzed by quantitative reverse transcriptase-PCR, enzyme-linked immunoassay, and IHC, and the data were statistically analyzed with respect to endoscopic and clinical parameters.


RESULTS
Forty-four patients had nonerosive and 51 erosive reflux diseases, respectively. Histology revealed higher chronic inflammation (P=0.04) and significant alterations of the intercellular spaces, basal cell hyperplasia, and length of papilla (P<0.05) in patients with GERD. Mucosal SLPI levels were comparable among antrum, cardia, and esophagus ranging from 95 to 165 pg/mug protein and were not affected by the presence of GERD, whereas esophageal SLPI-transcript levels were three-fold induced in patients with GERD (P=0.002). IHC identified epithelial cells as major cellular source of mucosal SLPI expression in normal cardiac and esophageal mucosa, whereas infiltrating immune cells contributed to the SLPI expression in chronically inflamed tissue.


CONCLUSIONS
GERD, a chemically induced inflammation, does not affect mucosal SLPI expression in gastroesophageal mucosa.
Wex
Thomas
T
Department of Gastroenterology, Hepatology, and Infectious Diseases, Otto-von-Guericke University, Magdeburg, Germany. thomas.wex@med.ovgu.de
Mönkemüller
Klaus
K
Kuester
Doerthe
D
Weise
Susanne
S
Kropf
Siegfried
S
Fry
Lucia C
LC
Stahr
Antje
A
Völkel
Simone
S
Roessner
Albert
A
Malfertheiner
Peter
P
D000293:Adolescent; D000328:Adult; D000368:Aged; D001706:Biopsy; D004943:Esophagogastric Junction / Q000378:metabolism; D004947:Esophagus / Q000378:metabolism* / Q000473:pathology; D005260:Female; D005764:Gastroesophageal Reflux / Q000378:metabolism* / Q000473:pathology; D005786:Gene Expression Regulation; D006801:Humans; D008297:Male; D008875:Middle Aged; D009092:Mucous Membrane / Q000378:metabolism / Q000473:pathology; D011446:Prospective Studies; D012313:RNA / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D053481:Secretory Leukocyte Peptidase Inhibitor / Q000235:genetics / Q000378:metabolism*; D055815:Young Adult
D053481:Secretory Leukocyte Peptidase Inhibitor; D012313:RNA