ArticleNature microbiology2022
Immunosuppression broadens evolutionary pathways to drug resistance and treatment failure during Acinetobacter baumannii pneumonia in mice.
Article in Nature microbiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 48 citations in OpenAlex.
- Simulating the host niche: balancing complexity and control in the experimental evolution of antibiotic resistance and pathoadaptation.Microbiology (Reading, England) · 2026Review
- Climate change and antimicrobial resistance.Nature reviews. Microbiology · 2026Review
- The power of ten: report from the 10th American Society for Microbiology Conference on Biofilms.Journal of bacteriology · 2026Article
- Antibacterial and Immunomodulatory Effects ofInternational journal of molecular sciences · 2026Article
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- A genomics-informed mechanism-based pharmacokinetic/pharmacodynamic model of cefiderocol and ceftazidime/avibactam against carbapenem-resistantAntimicrobial agents and chemotherapy · 2026Article
- Cell-selective multiplexed bioorthogonal noncanonical amino acid tagging for nascent proteomics.Nature chemical biology · 2026Article
- Resistance, heteroresistance, and fitness costs drive colistin treatment failure duringProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Immune imbalance markers: key factors in early recognition of multidrug-resistant bacterial infections in non-immunocompromised VAP patients.Frontiers in immunology · 2026Article
- Quantifying host-microbe interactions with bacterial lineage tracing.Science (New York, N.Y.) · 2026Review
- Deciphering the efficacy of staphyloxanthin-encapsulated niosomal nanovesicles to attenuate biofilm formation, quorum sensing, and meropenem persistence in Acinetobacter baumannii.BMC microbiology · 2025Article
- Scarless excision of an insertion sequence in the OmpK36 promoter restores meropenem susceptibility in a non-carbapenemase-producingEmerging microbes & infections · 2025Article
- Resistance, heteroresistance and fitness costs drive colistin treatment failure duringbioRxiv : the preprint server for biology · 2025Article
- Article
- Prevalence and Resistance Profiles ofAntibiotics (Basel, Switzerland) · 2025Review
- Loss of essential outer membrane functions causes drug hypersensitization inbioRxiv : the preprint server for biology · 2025Article
- The role of innate immunity, antibiotics, and bacteriophages in the course of bacterial infections and their treatment.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- A PP2A-mtATR-tBid axis links DNA damage-induced CIP2A degradation to apoptotic dormancy and therapeutic resistance in PDAC.Cancer letters · 2025Article
- The role of innate immunity, antibiotics, and bacteriophages in the course of bacterial infections and their treatment.bioRxiv : the preprint server for biology · 2025Article
- Distinct molecular characteristics and virulence profiles of carbapenem-resistantMicrobiology spectrum · 2025Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 1 country.
Funding
Abstract
Acinetobacter baumannii is increasingly refractory to antibiotic treatment in healthcare settings. As is true of most human pathogens, the genetic path to antimicrobial resistance (AMR) and the role that the immune system plays in modulating AMR during disease are poorly understood. Here we reproduced several routes to fluoroquinolone resistance, performing evolution experiments using sequential lung infections in mice that are replete with or depleted of neutrophils, providing two key insights into the evolution of drug resistance. First, neutropenic hosts acted as reservoirs for the accumulation of drug resistance during drug treatment. Selection for variants with altered drug sensitivity profiles arose readily in the absence of neutrophils, while immunocompetent animals restricted the appearance of these variants. Secondly, antibiotic treatment failure in the immunocompromised host was shown to occur without clinically defined resistance, an unexpected result that provides a model for how antibiotic failure occurs clinically in the absence of AMR. The genetic mechanism underlying both these results is initiated by mutations activating the drug egress pump regulator AdeL, which drives persistence in the presence of antibiotic. Therefore, antibiotic persistence mutations present a two-pronged risk during disease, causing drug treatment failure in the immunocompromised host while simultaneously increasing the emergence of high-level AMR.
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Registered trials
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.