Abstract
Antimicrobial peptides can protect the gastric mucosa from bacteria, but Helicobacter pylori (H. pylori) can equally colonize the gastric apparatus. To understand beta-defensin function in H. pylori-associated chronic gastritis, we investigated susceptibility, human beta-defensin mRNA expression, and DNA methylation changes to promoters in the gastric mucosa with or without H. pylori infection. We studied the expression of HBD2 (gene name DEFB4A), HBD3 (DEFB103A), and HBD4 (DEFB104) using real-time PCR in 15 control and 10 H. pylori infection patient gastric specimens. This study demonstrates that H. pylori infection is related to gastric enhancement of inducible HBD2, but inducible HBD3 and HBD4 expression levels remained unchanged. HBD2 gene methylation levels were overall higher in H. pylori-negative samples than in H. pylori-positive samples. We also assessed antimicrobial susceptibility using growth on blood agar. The H. pylori strain Tox+ was susceptible to all defensins tested and their analogs (3N, 3NI). These results show that HBD2 is involved in gastritis development driven by H. pylori, which facilitates the creation of an epigenetic field during H. pylori-associated gastric tumorigenesis.
Highlights
Chronic inflammation in specific organs is associated with increased cancer risk, including ulcerative colitis (UC)-associated colon cancer, liver cancer, and gastric cancer
We evaluated methylation levels of promoter CpG islands (CGI) of betadefensin genes (HBD2-4) in gastric biopsy specimens from 15 controls and 10 patients colonized by H. pylori
Methylation analysis of the HBD2 promoter regions was performed on genomic DNA extracted from human tissue gastric samples in 15 controls and 10 patients colonized by H. pylori, obtained from surgical specimens
Summary
Chronic inflammation in specific organs is associated with increased cancer risk, including ulcerative colitis (UC)-associated colon cancer, liver cancer, and gastric cancer. Storage of epigenetic modifications caused by chronic inflammation seems to correlate with tumor progression [1,2,3,4,5,6]. Chronic inflammation is correlated with the incidence of cancer development [7,8,9]. Chronic inflammation is triggered by infection of Helicobacter pylori (H. pylori) in the stomach, and it causes a predisposition in gastric cancer development [10,11].
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