Evidence map›Paper›PMID 36434690›Full record

ArticleMicrobiome2022

Colonocyte-derived lactate promotes E. coli fitness in the context of inflammation-associated gut microbiota dysbiosis.

Savannah J Taylor, Maria G Winter, Caroline C Gillis, Laice Alves da Silva, Amanda L Dobbins, Matthew K Muramatsu, Angel G Jimenez, Rachael B Chanin, Luisella Spiga, Ernesto M Llano and 5 more

Open access · goldAbstract readVideo-Audio Media
In one paragraph

Article in Microbiome, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.2field-weighted citation impact, top 4% 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

33 citing papers in PubMed, 48 citations in OpenAlex.

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    Review
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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

15 authors at 5 institutions in 2 countries.

Savannah J TaylorDepartment of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Maria G WinterDepartment of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Caroline C GillisDepartment of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Laice Alves da SilvaDepartamento de Clínica e Cirurgia Veterinárias, Escola de Veterinária, Universidade Federal de Minas Gerais, Belo Horizonte, MG, 31270, Brazil.
Amanda L DobbinsDepartment of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Matthew K MuramatsuDepartment of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Angel G JimenezDepartment of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Rachael B ChaninDepartment of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Luisella SpigaDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, USA.
Ernesto M LlanoDepartment of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Vivian K RojasDepartment of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Jiwoong KimDepartment of Population and Data Sciences, UT Southwestern Medical Center, Dallas, TX, 75390, USA.
Renato L SantosDepartamento de Clínica e Cirurgia Veterinárias, Escola de Veterinária, Universidade Federal de Minas Gerais, Belo Horizonte, MG, 31270, Brazil.
Wenhan ZhuDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, USA.
Sebastian E WinterDepartment of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, USA. sebwinter@ucdavis.edu.
The University of Texas Southwestern Medical Center · USUniversidade Federal de Minas Gerais · BRUniversity of California, Davis · USVanderbilt University Medical Center · USRiboMed Biotechnologies (United States) · US

Funding

UT Southwestern NORCP30DK127984 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI JONATHAN Charles COHEN · 2022 to 2026
$7.4M
MOLECULAR MICROBIOLOGY TRAINING GRANTT32AI007520 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI Julie K Pfeiffer · 1997 to 2026
$7.0M
UT GASTROENTEROLOGY/HEPATOLOGY RESEARCH TRAINING PROGRAMT32DK007745 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI Rodney E Infante · 1997 to 2026
$6.8M
Central metabolism of Salmonella in the inflamed gutR01AI118807 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI Sebastian E Winter · 2015 to 2026
$5.3M
Glutarate metabolism in SalmonellaR21AI166263 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI WINTER, SEBASTIAN E · 2021 to 2022
$444k
The role of host-derived reactive oxygen species in the outgrowth of Escherichia coli during non-infectious colitisF31DK121465 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI CHANIN, RACHAEL · 2020 to 2021
$46k
NIAID NIH HHS R01 AI118807NIAID NIH HHS R21 AI166263NIAID NIH HHS T32 AI007520NIDDK NIH HHS F31 DK121465NIDDK NIH HHS P30 DK127984NIDDK NIH HHS T32 DK007745
6 · The paper itself

Abstract

backgroundIntestinal inflammation disrupts the microbiota composition leading to an expansion of Enterobacteriaceae family members (dysbiosis). Associated with this shift in microbiota composition is a profound change in the metabolic landscape of the intestine. It is unclear how changes in metabolite availability during gut inflammation impact microbial and host physiology.

resultsWe investigated microbial and host lactate metabolism in murine models of infectious and non-infectious colitis. During inflammation-associated dysbiosis, lactate levels in the gut lumen increased. The disease-associated spike in lactate availability was significantly reduced in mice lacking the lactate dehydrogenase A subunit in intestinal epithelial cells. Commensal E. coli and pathogenic Salmonella, representative Enterobacteriaceae family members, utilized lactate via the respiratory L-lactate dehydrogenase LldD to increase fitness. Furthermore, mice lacking the lactate dehydrogenase A subunit in intestinal epithelial cells exhibited lower levels of inflammation in a model of non-infectious colitis.

conclusionsThe release of lactate by intestinal epithelial cells during gut inflammation impacts the metabolism of gut-associated microbial communities. These findings suggest that during intestinal inflammation and dysbiosis, changes in metabolite availability can perpetuate colitis-associated disturbances of microbiota composition. Video Abstract.

Indexed as

ColitisGastrointestinal MicrobiomeAnimalsDysbiosisEnterobacteriaceaeEscherichia coliInflammationLactate Dehydrogenase 5Lactic AcidMiceMice, Inbred C57BLLactate Dehydrogenase 5Lactic AcidGut inflammationHost-microbe interactionsLactate metabolism

Identifiers

PMID36434690
PMCPMC9701030
OpenAlexW4310295547

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.