Evidence map›Paper›PMID 35411114›Full record

ArticleNature biomedical engineering2022

An engineered live biotherapeutic for the prevention of antibiotic-induced dysbiosis.

Andrés Cubillos-Ruiz, Miguel A Alcantar, Nina M Donghia, Pablo Cárdenas, Julian Avila-Pacheco, James J Collins

Abstract read
PubMed Publisher
In one paragraph

Article in Nature biomedical engineering, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
8.0field-weighted citation impact, top 2% 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

54 citing papers in PubMed, 87 citations in OpenAlex.

  1. Review
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  4. Orally available designed miniproteins inhibit enterotoxigenicbioRxiv : the preprint server for biology · 2026
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  11. The gut as a central hub for multi-organ crosstalk in aging.Cellular and molecular life sciences : CMLS · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Andrés Cubillos-RuizInstitute for Medical Engineering and Science, and Synthetic Biology Center, Massachusetts Institute of Technology, Cambridge, MA, USA.
Miguel A AlcantarInstitute for Medical Engineering and Science, and Synthetic Biology Center, Massachusetts Institute of Technology, Cambridge, MA, USA.ORCID http://orcid.org/0000-0003-1189-2254
Nina M DonghiaWyss Institute for Biologically Inspired Engineering, Harvard University, Boston, MA, USA.
Pablo CárdenasDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.ORCID http://orcid.org/0000-0001-7015-0512
Julian Avila-PachecoBroad Institute of MIT and Harvard, Cambridge, MA, USA.ORCID http://orcid.org/0000-0001-9388-3946
James J CollinsInstitute for Medical Engineering and Science, and Synthetic Biology Center, Massachusetts Institute of Technology, Cambridge, MA, USA. jimjc@mit.edu.ORCID http://orcid.org/0000-0002-5560-8246
Broad Institute · USMassachusetts Institute of Technology · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antibiotic-induced alterations in the gut microbiota are implicated in many metabolic and inflammatory diseases, increase the risk of secondary infections and contribute to the emergence of antimicrobial resistance. Here we report the design and in vivo performance of an engineered strain of Lactococcus lactis that altruistically degrades the widely used broad-spectrum antibiotics β-lactams (which disrupt commensal bacteria in the gut) through the secretion and extracellular assembly of a heterodimeric β-lactamase. The engineered β-lactamase-expression system does not confer β-lactam resistance to the producer cell, and is encoded via a genetically unlinked two-gene biosynthesis strategy that is not susceptible to dissemination by horizontal gene transfer. In a mouse model of parenteral ampicillin treatment, oral supplementation with the engineered live biotherapeutic minimized gut dysbiosis without affecting the ampicillin concentration in serum, precluded the enrichment of antimicrobial resistance genes in the gut microbiome and prevented the loss of colonization resistance against Clostridioides difficile. Engineered live biotherapeutics that safely degrade antibiotics in the gut may represent a suitable strategy for the prevention of dysbiosis and its associated pathologies.

Indexed as

Clostridioides difficileDysbiosisAmpicillinAnimalsAnti-Bacterial Agentsbeta-LactamasesMiceAmpicillinAnti-Bacterial Agentsbeta-Lactamases

Identifiers

PMID35411114
OpenAlexW4223459026

What OpenQuestion holds

Textmetadata
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.