Investigation of the possibility of human-β defensin 2 (hBD2) as a molecular marker of gastric mucosal inflammation

Background/Aims: It has previously been reported that human-β defensin 2 (hBD2) has a physiological role as a proinflammatory mediator in gastric mucosal inflammation as well as an antimicrobial peptide for Helicobacter pylori (Hp). The present study was conducted to evaluate the possibility of hBD2 as a molecular marker of gastric mucosal inflammation. Methodology: The subjects were 40 A₁ to S₂ gastric ulcer patients, with or without Hp infection. Biopsy specimens of the mucosa were obtained endoscopically before and after the administration of lansoprazole (LPZ) (15mg/day) or famotidine (FAM) (40mg/day or 20mg/day), consecutively, and each set of samples was divided into two groups; one group was subjected to RT-PCR to assess the expression of hBD2, and the other was subjected to immunohistochemical analysis for evaluating the expression of CD68. Results: The expression of hBD2 was observed through the stage of gastric ulcer, from A₁ to S₁, regardless of the presence or absence of Hp infection, both before and after LPZ or FAM administration, and its intensity of expression decreasing as the number of CD68-positive cells decreased. The number of CD68-positive cells deceased as the severity of the ulcer increased from stage A₁ to S₂, regardless of the presence/absence of Hp infection. CD68-positive cells could hardly be observed in stage S2 gastric ulcers, in which hBD2 expression was also only scarcely noted. Conclusions: These results suggested the possibility that hBD2 may be a molecular marker of gastric mucosal inflammation, irrespective of the presence/absence of Hp infection.