ArticlePloS one2013
Gastric antimicrobial peptides fail to eradicate Helicobacter pylori infection due to selective induction and resistance.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 42 citations in OpenAlex.
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- Cathartocytosis: Jettisoning of cellular material during reprogramming of differentiated cells.Cell reports · 2025Article
- Breaking the resistance: integrative approaches with novel therapeutics against Klebsiella pneumoniae.Archives of microbiology · 2024Review
- IL-17 receptor A functions to help maintain barrier integrity and limit activation of immunopathogenic response toInfection and immunity · 2024Article
- Recent Advances in Vitamin D3 Intervention to EradicateJournal of multidisciplinary healthcare · 2024Review
- Immune Biology and Persistence of Helicobacter pylori in Gastric Diseases.Current topics in microbiology and immunology · 2023Article
- A review on the research progress on non-pharmacological therapy ofFrontiers in microbiology · 2023Review
- Lactobacilli Downregulate Transcription Factors inInternational journal of molecular sciences · 2022Article
- The Role of Antimicrobial Peptides as Antimicrobial and Antibiofilm Agents in Tackling the Silent Pandemic of Antimicrobial Resistance.Molecules (Basel, Switzerland) · 2022Review
- Multitalented Synthetic Antimicrobial Peptides and Their Antibacterial, Antifungal and Antiviral Mechanisms.International journal of molecular sciences · 2022Review
- Review
- Antimicrobial Peptides: A Potent Alternative to Antibiotics.Antibiotics (Basel, Switzerland) · 2021Review
- Antimicrobial peptides - Advances in development of therapeutic applications.Life sciences · 2020Review
- Decreased IL-17RB expression impairs CD11bCell death & disease · 2019Article
- β-Defensins in the Fight against Helicobacter pylori.Molecules (Basel, Switzerland) · 2017Review
- Microbes and Viruses Are Bugging the Gut in Celiac Disease. Are They Friends or Foes?Frontiers in microbiology · 2017Review
- IL-22-induced antimicrobial peptides are key determinants of mucosal vaccine-induced protection against H. pylori in mice.Mucosal immunology · 2017Article
- Host Antimicrobial Peptides in Bacterial Homeostasis and Pathogenesis of Disease.Antibiotics (Basel, Switzerland) · 2014Article
- Chemokines and antimicrobial peptides have a cag-dependent early response to Helicobacter pylori infection in primary human gastric epithelial cells.Infection and immunity · 2014Article
- Nontraditional therapies to treat Helicobacter pylori infection.Journal of microbiology (Seoul, Korea) · 2014Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlthough antimicrobial peptides protect mucus and mucosa from bacteria, Helicobacter pylori is able to colonize the gastric mucus. To clarify in which extend Helicobacter escapes the antimicrobial defense, we systematically assessed susceptibility and expression levels of different antimicrobial host factors in gastric mucosa with and without H. pylori infection. MATERIALS AND
methodsWe investigated the expression levels of HBD1 (gene name DEFB1), HBD2 (DEFB4A), HBD3 (DEFB103A), HBD4 (DEFB104A), LL37 (CAMP) and elafin (PI3) by real time PCR in gastric biopsy samples in a total of 20 controls versus 12 patients colonized with H. pylori. Immunostaining was performed for HBD2 and HBD3. We assessed antimicrobial susceptibility by flow cytometry, growth on blood agar, radial diffusion assay and electron microscopy.
resultsH. pylori infection was associated with increased gastric levels of the inducible defensin HBD2 and of the antiprotease elafin, whereas the expression levels of the constitutive defensin HBD1, inducible HBD3 and LL37 remained unchanged. HBD4 was not expressed in significant levels in gastric mucosa. H. pylori strains were resistant to the defensins HBD1 as well as to elafin, and strain specific minimally susceptible to HBD2, whereas HBD3 and LL37 killed all H. pylori strains effectively. We demonstrated the binding of HBD2 and LL37 on the surface of H. pylori cells. Comparing the antibacterial activity of extracts from H. pylori negative and positive biopsies, we found only a minimal killing against H. pylori that was not increased by the induction of HBD2 in H. pylori positive samples.
conclusionThese data support the hypothesis that gastric H. pylori evades the host defense shield to allow colonization.
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