Helicobacter pylori infection, but not low-dose aspirin, results in a local reduction of the secretory leukocyte protease inhibitor in gastroduodenal mucosa.
BACKGROUND
The secretory leukocyte protease inhibitor (SLPI) represents a multifunctional protein with mucosa-protective features. Helicobacter pylori and the usage of low-dose aspirin are two independent risk factors for the development of gastrointestinal diseases. Therefore, the effect of low-dose aspirin on gastrointestinal SLPI expression was analyzed in the context of H. pylori infection.


METHODS
The study included 20 volunteers (H. pylori positive and negative: n = 10) who received 2 x 50 mg aspirin/day for 7 days. H. pylori-positive subjects underwent eradication therapy and repeated the protocol. Gastroduodenoscopy was performed at day 0, 1, 3, and 7, and biopsies were obtained each from antrum, corpus, and duodenal bulb. SLPI expression was determined by quantitative reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA).


RESULTS
A reduction of antral SLPI levels, ranging between 582 (day 0) and 941 pg/10 microg protein (day 7), was determined in H. pylori-positive compared to H. pylori-negative and -eradicated subjects (1600-2050 pg/10 microg protein, ANOVA: p = .001-.045). No differences concerning aspirin were observed within the groups. SLPI levels in corpus and duodenal mucosa were neither affected by H. pylori nor low-dose aspirin. There was an inverse correlation between SLPI and H. pylori-induced inflammation (activity: r = -0.575, -0.69 to -0.43, p < .0001; chronicity: r = -0.54, -0.66 to -0.39, p < .0001) in antral mucosa only, whereas other locations as well as the usage of low-dose aspirin did not show an association between SLPI and inflammation.


CONCLUSIONS
H. pylori infection, but not the usage of low-dose aspirin, has a role in the down-regulation of antral SLPI levels.
Wex
Thomas
T
Department of Gastroenterology, Hepatology and Infectious Diseases, Tongji Medical College of Basic Medical Sciences, Huazhong University of Wuhan, China. thomas.wex@medizin.uni-magdeburg.de
Ye
Siying
S
Treiber
Gerhard
G
Vieth
Michael
M
Roessner
Albert
A
Malfertheiner
Peter
P
D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology / Q000627:therapeutic use; D001241:Aspirin / Q000494:pharmacology / Q000627:therapeutic use*; D004305:Dose-Response Relationship, Drug; D004386:Duodenum / Q000187:drug effects; D005260:Female; D005753:Gastric Mucosa / Q000187:drug effects / Q000378:metabolism*; D005756:Gastritis / Q000188:drug therapy / Q000382:microbiology / Q000473:pathology; D016481:Helicobacter Infections / Q000188:drug therapy* / Q000378:metabolism; D016480:Helicobacter pylori / Q000472:pathogenicity*; D006801:Humans; D007413:Intestinal Mucosa / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D011446:Prospective Studies; D053491:Proteinase Inhibitory Proteins, Secretory; D011506:Proteins / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D053481:Secretory Leukocyte Peptidase Inhibitor
D000894:Anti-Inflammatory Agents, Non-Steroidal; D053491:Proteinase Inhibitory Proteins, Secretory; D011506:Proteins; C506814:SLPI protein, human; D053481:Secretory Leukocyte Peptidase Inhibitor; D001241:Aspirin