{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,11,22]],"date-time":"2023-11-22T17:00:26Z","timestamp":1700672426013},"reference-count":37,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2006,1,18]],"date-time":"2006-01-18T00:00:00Z","timestamp":1137542400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Helicobacter"],"published-print":{"date-parts":[[2006,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p><jats:bold>Background:\u2002<\/jats:bold> The secretory leukocyte protease inhibitor (SLPI) represents a multifunctional protein with mucosa\u2010protective features. <jats:italic>Helicobacter pylori<\/jats:italic> and the usage of low\u2010dose aspirin are two independent risk factors for the development of gastrointestinal diseases. Therefore, the effect of low\u2010dose aspirin on gastrointestinal SLPI expression was analyzed in the context of <jats:italic>H. pylori<\/jats:italic> infection.<\/jats:p><jats:p><jats:bold>Material and Methods:\u2002<\/jats:bold> The study included 20 volunteers (<jats:italic>H. pylori<\/jats:italic> positive and negative: n\u00a0=\u00a010) who received 2\u00a0\u00d7\u00a050\u00a0mg aspirin\/day for 7\u00a0days. <jats:italic>H. pylori<\/jats:italic>\u2010positive 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\u2010polymerase chain reaction (RT\u2010PCR) and enzyme\u2010linked immunosorbent assay (ELISA).<\/jats:p><jats:p><jats:bold>Results:\u2002<\/jats:bold> A reduction of antral SLPI levels, ranging between 582 (day 0) and 941\u00a0pg\/10\u00a0\u00b5g protein (day 7), was determined in <jats:italic>H. pylori<\/jats:italic>\u2010positive compared to <jats:italic>H. pylori<\/jats:italic>\u2010negative and \u2010eradicated subjects (1600\u20132050\u00a0pg\/10\u00a0\u00b5g protein, ANOVA: <jats:italic>p<\/jats:italic>\u00a0=\u00a0.001\u2013.045). No differences concerning aspirin were observed within the groups. SLPI levels in corpus and duodenal mucosa were neither affected by <jats:italic>H.\u00a0pylori<\/jats:italic> nor low\u2010dose aspirin. There was an inverse correlation between SLPI and <jats:italic>H. pylori<\/jats:italic>\u2010induced inflammation (activity: <jats:italic>r<\/jats:italic>\u00a0=\u00a0\u22120.575, \u22120.69 to \u22120.43, <jats:italic>p<\/jats:italic>\u00a0&lt;\u00a0.0001; chronicity: <jats:italic>r<\/jats:italic>\u00a0=\u00a0\u22120.54, \u22120.66 to \u22120.39, <jats:italic>p<\/jats:italic>\u00a0&lt;\u00a0.0001) in antral mucosa only, whereas other locations as well as the usage of low\u2010dose aspirin did not show an association between SLPI and inflammation.<\/jats:p><jats:p><jats:bold>Conclusions:\u2002<\/jats:bold>  <jats:italic>H. pylori<\/jats:italic> infection, but not the usage of low\u2010dose aspirin, has a role in the down\u2010regulation of antral SLPI 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