Helicobacter · 2012
Differential expression of human beta defensin 2 and 3 in gastric mucosa of Helicobacter pylori-infected individuals.
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Bauer Bianca, Wex Thomas, Kuester Doerthe, Meyer Thomas, Malfertheiner Peter
Аннотация
BACKGROUND: Antimicrobial peptides are key players of initial innate immune responses to human pathogens. Two major representatives, the human beta defensin 2 and 3 (hBD2 and hBD3), are both known to be regulated by, and to affect viability of, Helicobacter pylori. Previously, it was demonstrated in vitro that H. pylori actively abrogates hBD3 expression during prolonged infections. Here, we comprehensively assessed hBD2 and hBD3 expression ex vivo in the gastric mucosa of healthy individuals.
MATERIALS AND METHODS: Twenty volunteers (H. pylori positive and H. pylori negative: n = 10) were enrolled. Helicobacter pylori-positive subjects underwent eradication therapy and repeated the protocol. Expression of both defensins was assessed by quantitative RT-PCR and ELISA, and correlated with histopathologic degree of gastritis.
RESULTS: hBD2 and hBD3 were found to be ubiquitously expressed in all three groups. In general, hBD2 levels were elevated in relation to H. pylori infection (up to 40-fold). This upregulation correlated with degree of gastritis in corpus and antrum. In contrast, hBD3 protein levels were significantly decreased, while corresponding mRNA amounts remained unchanged. Eradication therapy led to normalization of mucosal hBD2 expression, while hBD3 expression demonstrated high interindividual variations among individuals.
CONCLUSIONS: Both defensins are ubiquitously but differentially expressed in gastric mucosa in relation to H. pylori infection. Ex vivo data support the notion that H. pylori infection is associated with reduced hBD3 expression in chronic active gastritis.
MATERIALS AND METHODS: Twenty volunteers (H. pylori positive and H. pylori negative: n = 10) were enrolled. Helicobacter pylori-positive subjects underwent eradication therapy and repeated the protocol. Expression of both defensins was assessed by quantitative RT-PCR and ELISA, and correlated with histopathologic degree of gastritis.
RESULTS: hBD2 and hBD3 were found to be ubiquitously expressed in all three groups. In general, hBD2 levels were elevated in relation to H. pylori infection (up to 40-fold). This upregulation correlated with degree of gastritis in corpus and antrum. In contrast, hBD3 protein levels were significantly decreased, while corresponding mRNA amounts remained unchanged. Eradication therapy led to normalization of mucosal hBD2 expression, while hBD3 expression demonstrated high interindividual variations among individuals.
CONCLUSIONS: Both defensins are ubiquitously but differentially expressed in gastric mucosa in relation to H. pylori infection. Ex vivo data support the notion that H. pylori infection is associated with reduced hBD3 expression in chronic active gastritis.