Evidence map›Paper›PMID 37908118›Full record

ArticleGut microbes2023

A metagenomic analysis for combination therapy of multiple classes of antibiotics on the prevention of the spread of antibiotic-resistant genes.

Matthew Igo, Lei Xu, Ashok Krishna, Sharron Stewart, Lin Xu, Zhihua Li, James L Weaver, Heather Stone, Leonard Sacks, Timothy Bensman and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Gut microbes, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.6field-weighted citation impact, top 29% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. bioRxiv : the preprint server for biology · 2026
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 1 institution in 1 country.

Matthew IgoDivision of Applied Regulatory Science, Office of Clinical Pharmacology, Office of Translational Sciences, Center for Drug Evaluation and Research, U. S. Food and Drug Administration, Silver Spring, MD, USA.
Lei XuDivision of Applied Regulatory Science, Office of Clinical Pharmacology, Office of Translational Sciences, Center for Drug Evaluation and Research, U. S. Food and Drug Administration, Silver Spring, MD, USA.
Ashok KrishnaDivision of Applied Regulatory Science, Office of Clinical Pharmacology, Office of Translational Sciences, Center for Drug Evaluation and Research, U. S. Food and Drug Administration, Silver Spring, MD, USA.
Sharron StewartDivision of Applied Regulatory Science, Office of Clinical Pharmacology, Office of Translational Sciences, Center for Drug Evaluation and Research, U. S. Food and Drug Administration, Silver Spring, MD, USA.
Lin XuDivision of Applied Regulatory Science, Office of Clinical Pharmacology, Office of Translational Sciences, Center for Drug Evaluation and Research, U. S. Food and Drug Administration, Silver Spring, MD, USA.
Zhihua LiDivision of Applied Regulatory Science, Office of Clinical Pharmacology, Office of Translational Sciences, Center for Drug Evaluation and Research, U. S. Food and Drug Administration, Silver Spring, MD, USA.
James L WeaverDivision of Applied Regulatory Science, Office of Clinical Pharmacology, Office of Translational Sciences, Center for Drug Evaluation and Research, U. S. Food and Drug Administration, Silver Spring, MD, USA.
Heather StoneOffice of Medical Policy, Center for Drug Evaluation and Research, U. S. Food and Drug Administration, Silver Spring, MD, USA.
Leonard SacksOffice of Medical Policy, Center for Drug Evaluation and Research, U. S. Food and Drug Administration, Silver Spring, MD, USA.
Timothy BensmanDivision of Infectious Disease Pharmacology, Office of Clinical Pharmacology, Office of Translational Sciences, Center for Drug Evaluation and Research, U. S. Food and Drug Administration, Silver Spring, MD, USA.
Jeffry FlorianDivision of Applied Regulatory Science, Office of Clinical Pharmacology, Office of Translational Sciences, Center for Drug Evaluation and Research, U. S. Food and Drug Administration, Silver Spring, MD, USA.
Rodney RouseDivision of Applied Regulatory Science, Office of Clinical Pharmacology, Office of Translational Sciences, Center for Drug Evaluation and Research, U. S. Food and Drug Administration, Silver Spring, MD, USA.
Xiaomei HanDivision of Applied Regulatory Science, Office of Clinical Pharmacology, Office of Translational Sciences, Center for Drug Evaluation and Research, U. S. Food and Drug Administration, Silver Spring, MD, USA.ORCID 0000-0002-2549-9122
United States Food and Drug Administration · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antibiotics used systemically to treat infections may have off-target effects on the gut microbiome, potentially resulting in the emergence of drug-resistant bacteria or selection of pathogenic species. These organisms may present a risk to the host and spread to the environment with a risk of transmission in the community. To investigate the risk of emergent antibiotic resistance in the gut microbiome following systemic treatment with antibiotics, this metagenomic analysis project used next-generation sequencing, a custom-built metagenomics pipeline, and differential abundance analysis to study the effect of antibiotics (ampicillin, ciprofloxacin, and fosfomycin) in monotherapy and different combinations at high and low doses, to determine the effect on resistome and taxonomic composition in the gut of Balb/c mice. The results showed that low-dose monotherapy treatments showed little change in microbiome composition but did show an increase in expression of many antibiotic-resistant genes (ARGs) posttreatment. Dual combination treatments allowed the emergence of some conditionally pathogenic bacteria and some increase in the abundance of ARGs despite a general decrease in microbiota diversity. Triple combination treatment was the most successful in inhibiting emergence of relevant opportunistic pathogens and completely suppressed all ARGs after 72 h of treatment. The relative abundances of mobile genetic elements that can enhance transmission of antibiotic resistance either decreased or remained the same for combination therapy while increasing for low-dose monotherapy. Combination therapy prevented the emergence of ARGs and decreased bacterial diversity, while low-dose monotherapy treatment increased ARGs and did not greatly change bacterial diversity.

Indexed as

Gastrointestinal MicrobiomeMicrobiotaAmpicillinAnimalsAnti-Bacterial AgentsBacteriaCiprofloxacinGenes, BacterialMiceAmpicillinAnti-Bacterial AgentsCiprofloxacinantibiotic-resistant genesantibioticscombination therapyMetagenomic analysis

Identifiers

PMID37908118
PMCPMC10621307
OpenAlexW4388139007

What OpenQuestion holds

Textmetadata
LicenceCC0
Read underepoch 390

Registered trials

None linked

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.