Evidence map›Paper›PMID 41136898›Full record

ArticleBMC genomics2025

Prevalence of oxalotrophy in the human microbiome.

Thomas Junier, Fabio Palmieri, Niki D Ubags, Aurélien Trompette, Angela Koutsokera, Pilar Junier, Marco Pagni, Samuel Neuenschwander

Abstract read
In one paragraph

Article in BMC genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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, 1 synthesis or guideline pooled it.

  1. Pooled it
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

8 authors.

Thomas JunierVital-IT, Swiss Institute of Bioinformatics, Lausanne, Switzerland. thomas.junier@sib.swiss.ORCID http://orcid.org/0000-0002-4015-5969
Fabio PalmieriLaboratoire de Microbiologie, University of Neuchâtel, Neuchâtel, Switzerland.ORCID http://orcid.org/0000-0002-5241-6898
Niki D UbagsDivision of Pulmonary Medicine, Lausanne University Hospital (CHUV) and University of Lausanne, Lausanne, Switzerland.ORCID http://orcid.org/0000-0002-0177-4134
Aurélien TrompetteDivision of Pulmonary Medicine, Lausanne University Hospital (CHUV) and University of Lausanne, Lausanne, Switzerland.ORCID http://orcid.org/0000-0001-5244-0823
Angela KoutsokeraDivision of Pulmonary Medicine, Lausanne University Hospital (CHUV) and University of Lausanne, Lausanne, Switzerland.ORCID http://orcid.org/0000-0003-1227-1679
Pilar JunierLaboratoire de Microbiologie, University of Neuchâtel, Neuchâtel, Switzerland.ORCID http://orcid.org/0000-0002-8618-3340
Marco PagniVital-IT, Swiss Institute of Bioinformatics, Lausanne, Switzerland.ORCID http://orcid.org/0000-0001-9292-9463
Samuel NeuenschwanderVital-IT, Swiss Institute of Bioinformatics, Lausanne, Switzerland.ORCID http://orcid.org/0000-0002-4080-5546

Funding

Gebert Rüf Stiftung GRS-064/18Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung 40B2-0_194701
6 · The paper itself

Abstract

backgroundIncomplete degradation of oxalate, a compound commonly found in the diet, can lead to disease in humans, particularly affecting the kidneys. The concentration of oxalate in the body depends on several factors, one of which is intestinal absorption-an aspect influenced by oxalotrophy among enteric bacteria. Despite its potential significance, oxalotrophy in the human microbiome remains poorly understood.

resultsIn this study, we conducted a systematic search for the co-occurrence of three key oxalotrophy genes-frc, oxc, and oxlT. We developed and validated specific conservation models for each gene and applied them to genomes and metagenomes associated with the human digestive tract, oral cavity, and lungs. Our analysis revealed that oxalotrophy, defined as the capacity to use oxalate as an energy source, is a rare metabolic trait predominantly confined to the gut. We also found evidence that this capacity can be acquired via horizontal gene transfer.

conclusionsWhile oxalotrophy is relatively uncommon, the broader capacity for oxalate degradation is more widespread. Notably, the genes frc and oxc are frequently found in close proximity within genomes, suggesting a selective advantage for organisms possessing this capability. Incomplete degradation of oxalate, a compound commonly found in the diet, can cause disease in humans, particularly affecting the kidney. Its concentration in the body depends on several factors, one of which is intestinal absorption, which is itself affected by oxalotrophy among enteric bacteria. Oxalotrophy in the human microbiome is poorly known. In this study, we perform a systematic search for the simultaneous presence of the three oxalotrophy genes, namely frc, oxc and oxlT. Thanks to the construction and validation of specific conservation models for all three genes, we were able to search for oxalotrophy in genomes and metagenomes associated with the human digestive tract, oral cavity, and lungs. We report that oxalotrophy-the capacity to use oxalate as an energy source-is a rare metabolic trait, mostly confined to the gut, and also find evidence that it can be acquired by horizontal gene transfer. By contrast, the capacity for oxalate degradation is more widespread, and two genes responsible for it (frc and oxc) are almost always close together in the genome, suggesting selection pressure.

Indexed as

BacteriaMicrobiotaOxalatesGene Transfer, HorizontalHumansMetagenomeOxalatesHuman microbiomeOxalate-related diseaseOxalotrophy

Identifiers

PMID41136898
PMCPMC12551280

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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.