Open AccessBeta-defensins and analogs in Helicobacter pylori infections: mRNA expression levels, DNA methylation, and antibacterial activity
Author(s) -
Raffaela Pero,
Tiziana Angrisano,
Mariarita Brancaccio,
Annarita Falanga,
Lucia Lombardi,
Francesco Natale,
Sonia Laneri,
Barbara Lombardo,
Stefania Galdiero,
Olga Scudiero
Publication year - 2019
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0222295
Subject(s) - beta defensin , helicobacter pylori , dna methylation , gastritis , gastric mucosa , biology , methylation , epigenetics , microbiology and biotechnology , chronic gastritis , defensin , gene expression , gene , antimicrobial , stomach , genetics , biochemistry
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.