ArticleNature communications2025
Human neutrophil α-defensin HNP1 interacts with bacterial OmpA to promote Acinetobacter baumannii biofilm formation.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- Computer-Aided Design ofACS medicinal chemistry letters · 2026Article
- New Insights intoPathogens (Basel, Switzerland) · 2026Review
- Multidrug resistant Acinetobacter baumannii shows epidemiology and transmission patterns in a China tertiary hospital ICU.Scientific reports · 2026Article
- Breaking disulfide bonds in a weakly bactericidal α-defensin unleashes a potent antimicrobial peptide with an altered conformation.PLoS pathogens · 2026Article
- Inside Enemy Lines: Adhesion, Invasion, and Intracellular Persistence ofPathogens (Basel, Switzerland) · 2026Review
- Acinetobacter baumannii-rare virulence factors and pathogenesis: the impact of biofilm associated protein (Bap), outer membrane vesicles, and iron acquisition system.Archives of microbiology · 2025Review
- Human neutrophil α-defensin HNP1 interacts with bacterial cell wall components to promote biofilm formation byBiofilm · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Acinetobacter baumannii is the causative agent of a wide range of nosocomial and community-acquired infections that remain extremely difficult to treat due largely to its antibiotic resistance contributed, in part, by biofilm formation. We find that the prototypic human neutrophil α-defensin HNP1, present in the bronchoalveolar lavage fluids from Acinetobacter baumannii-infected patients, promotes Acinetobacter baumannii biofilm formation through interactions with the bacterial outer membrane protein OmpA. As a result of HNP1-enhanced biofilm formation, Acinetobacter baumannii becomes more tolerant to antibiotics and more readily colonizes host cells and tissues. These unexpected findings contrast the protective roles HNP1 plays in innate immunity against microbial infection, showcasing an example of the host-pathogen arms race where a host defense peptide is exploited by a microbe for pathogenicity.
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Registered trials
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