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Abstract
Objective. Alpha-1 protease inhibitor (α1-PI) is the major circulating serine protease inhibitor. The purpose of the study was to investigate α1-PI expression in gastroduodenal mucosa and blood with respect to two major etiological risk factors for gastroduodenal diseases, Helicobacter pylori infection and intake of low-dose aspirin. Material and methods. Twenty volunteers (H. pylori-positive and -negative: n=10) received 2×50 mg aspirin/day for 7 days. H. pylori-positive subjects underwent eradication therapy and repeated the protocol. Blood and tissue samples were obtained on days 0, 1, 3 and 7; α1-PI levels were determined by enzyme-linked immunosorbent assay (ELISA) and quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) and analyzed for histopathological findings. Results. Mucosal α1-PI expression was between 30 and 75 pg/10 µg total protein in H. pylori-negative subjects, and found to be similar in antral, corpus and duodenal mucosa. In H. pylori-infected subjects, α1-PI levels were significantly increased in the antrum (mean: 111 versus 37.4 pg/10 µg protein; p=0.019), whereas corresponding levels in the corpus, duodenum and sera were unchanged. Alpha-1-PI transcript levels were similarly induced in H. pylori-infected subjects (0.13±0.15 versus 0.027±0.043 a.u. (arbitrary units), p=0.018). Immunohistochemistry demonstrated that infiltrating immune cells and antral surface epithelium contributed to elevated α1-PI expression in H. pylori-infected subjects. The concomitant use of low-dose aspirin did not change mucosal α1-PI levels, but led to a 2-fold increase in α1-PI levels in sera independently of the H. pylori status (p<0.009). Conclusions. Antral α1-PI expression is specifically induced by H. pylori infection, suggesting a pathophysiological role of this protease inhibitor in the upper gastrointestinal tract, whereas low-dose aspirin led to an increase in systemic α1-PI levels.