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Beta-defensins and analogs in Helicobacter pylori infections: mRNA expression levels, DNA methylation, and antibacterial activity


Autoři: Raffaela Pero aff001;  Tiziana Angrisano aff003;  Mariarita Brancaccio aff004;  Annarita Falanga aff005;  Lucia Lombardi aff006;  Francesco Natale aff003;  Sonia Laneri aff005;  Barbara Lombardo aff001;  Stefania Galdiero aff005;  Olga Scudiero aff001
Působiště autorů: Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università degli Studi di Napoli “Federico II”, Napoli, Italy aff001;  Task Force sugli Studi del Microbioma, Università degli Studi di Napoli “Federico II”, Napoli, Italy aff002;  Dipartimento di Biologia, Università degli Studi di Napoli “Federico II”, Napoli, Italy aff003;  Dipartimento di Biologia ed Evoluzione degli Organismi Marini, Stazione Zoologica Anton Dohrn, Napoli, Italy aff004;  Dipartimento di Farmacia, Università degli Studi di Napoli “Federico II”, Napoli, Italy aff005;  Dipartimento di Agraria, Università degli Studi di Napoli “Federico II”, Napoli, Italy aff006;  CEINGE-Biotecnologie Avanzate Scarl, Napoli, Italy aff007
Vyšlo v časopise: PLoS ONE 14(9)
Kategorie: Research Article
doi: https://doi.org/10.1371/journal.pone.0222295

Souhrn

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.

Klíčová slova:

Biology and life sciences – Cell biology – Chromosome biology – Chromatin – Chromatin modification – DNA methylation – Genetics – Epigenetics – DNA modification – Gene expression – DNA – Biochemistry – Nucleic acids – Microbiology – Medical microbiology – Microbial pathogens – Bacterial pathogens – Helicobacter pylori – Microbial control – Antimicrobials – Organisms – Bacteria – Helicobacter – Medicine and health sciences – Pathology and laboratory medicine – Pathogens – Gastroenterology and hepatology – Gastritis – Gastrointestinal infections – Immunology – Immune response – Inflammation – Diagnostic medicine – Signs and symptoms – Pharmacology – Drugs – Research and analysis methods – Database and informatics methods – Bioinformatics – Sequence analysis – DNA sequence analysis


Zdroje

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