ArticleThe Journal of infectious diseases2015
Host fate is rapidly determined by innate effector-microbial interactions during Acinetobacter baumannii bacteremia.
Article in The Journal of infectious diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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Who cites it
74 citing papers in PubMed, 97 citations in OpenAlex.
- Using the Damage Response Framework as a Lens to Discuss Acinetobacter baumannii Host-Pathogen Interactions: A Narrative Review and a Call to Action.Infectious diseases and therapy · 2026Review
- Cross-Species Dissemination of Pandrug-ResistantMicroorganisms · 2026Article
- Mobilization of the AbGRI4 resistance island inMicrobiology spectrum · 2026Article
- Resistance, heteroresistance, and fitness costs drive colistin treatment failure duringProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Characterizing the in vitro and in vivo effect of bicarbonate on azithromycin activity against Acinetobacter baumannii.PloS one · 2026Article
- Modulation of macrophage survival duringFrontiers in cellular and infection microbiology · 2026Review
- Resistance, heteroresistance and fitness costs drive colistin treatment failure duringbioRxiv : the preprint server for biology · 2025Article
- Antivirulence drugs against Acinetobacter baumannii: where do they stand?World journal of microbiology & biotechnology · 2025Review
- A chronic Acinetobacter baumannii pneumonia model to study long-term virulence factors, antibiotic treatments, and polymicrobial infections.Nature communications · 2025Article
- HypervirulentAntibiotics (Basel, Switzerland) · 2025Review
- Humoral response induced after intranasal vaccination with heat inactivatedFrontiers in immunology · 2025Article
- The intricacies ofFrontiers in microbiology · 2025Review
- Multidrug resistantCurrent research in microbial sciences · 2025Review
- OMP38 of Carbapenem-Resistant Acinetobacter Baumannii-Mediated mtDNA Release Activates the cGAS-STING Signaling to Induce Inflammatory Response.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Polymyxins retainAntimicrobial agents and chemotherapy · 2024Article
- Experimental evolution under different nutritional conditions changes the genomic architecture and virulence of Acinetobacter baumannii.Communications biology · 2024Article
- The Comparative Characterization of a HypervirulentInternational journal of molecular sciences · 2024Article
- Development and Evaluation of an Immunoinformatics-Based Multi-Peptide Vaccine againstVaccines · 2024Article
- Population pharmacokinetics and humanized dosage regimens matching the peak, area, trough, and range of amikacin plasma concentrations in immune-competent murine bloodstream and lung infection models.Antimicrobial agents and chemotherapy · 2024Article
- Clinical assays rapidly predict bacterial susceptibility to monoclonal antibody therapy.JCI insight · 2024Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundAcinetobacter baumannii is one of the most antibiotic-resistant pathogens. Defining mechanisms driving pathogenesis is critical to enable new therapeutic approaches.
methodsWe studied virulence differences across a diverse panel of A. baumannii clinical isolates during murine bacteremia to elucidate host-microbe interactions that drive outcome.
resultsWe identified hypervirulent strains that were lethal at low intravenous inocula and achieved very high early, and persistent, blood bacterial densities. Virulent strains were nonlethal at low inocula but lethal at 2.5-fold higher inocula. Finally, relatively avirulent (hypovirulent) strains were nonlethal at 20-fold higher inocula and were efficiently cleared by early time points. In vivo virulence correlated with in vitro resistance to complement and macrophage uptake. Depletion of complement, macrophages, and neutrophils each independently increased bacterial density of the hypovirulent strain but insufficiently to change lethality. However, disruption of all 3 effector mechanisms enabled early bacterial densities similar to hypervirulent strains, rendering infection 100% fatal.
conclusionsThe lethality of A. baumannii strains depends on distinct stages. Strains resistant to early innate effectors are able to establish very high early bacterial blood density, and subsequent sustained bacteremia leads to Toll-like receptor 4-mediated hyperinflammation and lethality. These results have important implications for translational efforts to develop therapies that modulate host-microbe interactions.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.