Expression of human beta-defensin 2 (hBD-2) in Helicobacter pylori inducedgastritis: antibacterial effect of hBD-2 against Helicobacter pylori

Background-Human beta -defensin 2 (hBD-2) plays a role in the innate defenc e system at mucosal surfaces. Colonisation of Helicobacter pylori in the st omach is an important pathological factor in gastrointestinal illnesses, in cluding gastritis, peptic ulcer, and gastric adenocarcinoma. Aims-To evaluate the antibacterial role of hBD-2 against H pylori infection in the gastric mucosa. Subjects-Biopsied gastric mucosa specimens from H pylori positive (n=6) and H pylori negative (n=6) individuals were used. H pylori was determined by the presence of urease activity and microscopic examination. Methods-The specimens were examined for hBD-2 expression by reverse transcr iption-polymerase chain reaction (RT-PCR), immunohistochemistry, and in sit u hybridisation. The antibacterial effect of hBD-2 against H pylori was eva luated by the number of colony forming units of H pylori after incubation w ith 0, 10(-9), 10(-8), 10(-7), 10(-6), or 10(-5)M of hBD-2 peptide. Results-All six H pylori positive specimens expressed a high level of hBD-2 mRNA while hBD-2 mRNA was not detected in the H pylori negative specimens by RT-PCR. Immunohistochemistry using anti-hBD-2 antiserum revealed that hB D-2 was expressed in the surface epithelium of H pylori infected specimens. In gastric specimens obtained after H pylori eradication, hBD-2 immunoreac tivity had dramatically decreased. In situ hybridisation confirmed that hBD -2 transcripts were localised in the epithelium of H pylori infected gastri c specimens. Incubation with hBD-2 reduced the growth rate of cultured H py lori in a dose dependent manner, and incubation with 10(-5) M hBD-2 complet ely inhibited the proliferation of H pylori. Conclusions-H pylori infection induces hBD-2 expression in the human gastri c epithelium. hBD-2 inhibited the growth of H pylori in vitro, suggesting t hat hBD-2 plays an antibacterial role in H pylori induced gastritis.