Evidence map›Paper›PMID 36197997›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2022

Stunted children display ectopic small intestinal colonization by oral bacteria, which cause lipid malabsorption in experimental models.

Pascale Vonaesch, João R Araújo, Jean-Chrysostome Gody, Jean-Robert Mbecko, Hugues Sanke, Lova Andrianonimiadana, Tanteliniaina Naharimanananirina, Synthia Nazita Ningatoloum, Sonia Sandrine Vondo, Privat Bolmbaye Gondje and 12 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.3field-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

27 citing papers in PubMed, 43 citations in OpenAlex.

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  16. Current Understanding ofCurrent tropical medicine reports · 2024
    Article
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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

22 authors at 7 institutions in 7 countries.

Pascale VonaeschUnité de Pathogénie Microbienne Moléculaire, Institut Pasteur, 75015 Paris, France.
João R AraújoUnité de Pathogénie Microbienne Moléculaire, Institut Pasteur, 75015 Paris, France.
Jean-Chrysostome GodyComplexe Hospitalo-Universitaire Pédiatrique de Bangui, Bangui, Central African Republic.
Jean-Robert MbeckoLaboratoire d'Analyse Médicale, Institut Pasteur de Bangui, Bangui, Central African Republic.
Hugues SankeLaboratoire d'Analyse Médicale, Institut Pasteur de Bangui, Bangui, Central African Republic.
Lova AndrianonimiadanaUnité de Bactériologie Expérimentale, Institut Pasteur de Madagascar, Antananarivo, 101 Madagascar.
Tanteliniaina NaharimanananirinaCentre Hospitalier Universitaire Joseph Ravoahangy Andrianavalona; Antananarivo, 101 Madagascar.
Synthia Nazita NingatoloumComplexe Hospitalo-Universitaire Pédiatrique de Bangui, Bangui, Central African Republic.
Sonia Sandrine VondoComplexe Hospitalo-Universitaire Pédiatrique de Bangui, Bangui, Central African Republic.
Privat Bolmbaye GondjeComplexe Hospitalo-Universitaire Pédiatrique de Bangui, Bangui, Central African Republic.
Andre Rodriguez-PozoUnité de Pathogénie Microbienne Moléculaire, Institut Pasteur, 75015 Paris, France.
Maheninasy RakotondrainipianaUnité d'Epidémiologie et de Recherche Clinique, Institut Pasteur de Madagascar, Antananarivo, 101 Madagascar.
Kaleb Jephté Estimé KandouLaboratoire de Coprologie Fonctionnelle, Assistance Publique-Hôpitaux de Paris, Hôpital Pitié-Salpêtrière, Paris, 75013 France.
Alison NestoretUnité d'Epidémiologie, Institut Pasteur de Bangui, Bangui, Central African Republic.
Nathalie KapelUnité d'Epidémiologie, Institut Pasteur de Bangui, Bangui, Central African Republic.
Serge Ghislain DjorieLaboratoire de Coprologie Fonctionnelle, Assistance Publique-Hôpitaux de Paris, Hôpital Pitié-Salpêtrière, Paris, 75013 France.
B Brett FinlayMichael Smith Laboratory, Department of Microbiology and Immunology, University of British Columbia, Vancouver, BC, BC V6T 1Z4 Canada.
Laura Wegener ParfreyBiodiversity Center, University of British Columbia, Vancouver, BC, BC V6T 1Z4 Canada.
Jean-Marc CollardComplexe Hospitalo-Universitaire Pédiatrique de Bangui, Bangui, Central African Republic.
Rindra Vatosoa RandremananaUnité d'Epidémiologie et de Recherche Clinique, Institut Pasteur de Madagascar, Antananarivo, 101 Madagascar.
Philippe J SansonettiUnité de Pathogénie Microbienne Moléculaire, Institut Pasteur, 75015 Paris, France.ORCID 0000-0001-7542-4527
Afribiota Investigators
Shanghai Institute of Nutrition and Health · CNInstitut Pasteur · FRInstitut Pasteur de Bangui · CFUniversity of Bangui · CFInstitut Pasteur de Madagascar · MGUniversity of British Columbia · CASorbonne Université · FR

Funding

Howard Hughes Medical Institute
6 · The paper itself

Abstract

Environmental enteric dysfunction (EED) is an inflammatory syndrome postulated to contribute to stunted child growth and to be associated with intestinal dysbiosis and nutrient malabsorption. However, the small intestinal contributions to EED remain poorly understood. This study aimed to assess changes in the proximal and distal intestinal microbiota in the context of stunting and EED and to test for a causal role of these bacterial isolates in the underlying pathophysiology. We performed a cross-sectional study in two African countries recruiting roughly 1,000 children aged 2 to 5 years and assessed the microbiota in the stomach, duodenum, and feces. Upper gastrointestinal samples were obtained from stunted children and stratified according to stunting severity. Fecal samples were collected. We then investigated the role of clinical isolates in EED pathophysiology using tissue culture and animal models. We find that small intestinal bacterial overgrowth (SIBO) is extremely common (>80%) in stunted children. SIBO is frequently characterized by an overgrowth of oral bacteria, leading to increased permeability and inflammation and to replacement of classical small intestinal strains. These duodenal bacterial isolates decrease lipid absorption in both cultured enterocytes and mice, providing a mechanism by which they may exacerbate EED and stunting. Further, we find a specific fecal signature associated with the EED markers fecal calprotectin and alpha-antitrypsin. Our study shows a causal implication of ectopic colonization of oral bacterial isolated from the small intestine in nutrient malabsorption and gut leakiness in vitro. These findings have important therapeutic implications for modulating the microbiota through microbiota-targeted interventions.

Indexed as

Gastrointestinal MicrobiomeGrowth DisordersIntestine, SmallLipidsMouthAnimalsBacteriaChild, PreschoolCross-Sectional StudiesHumansLeukocyte L1 Antigen ComplexLipid MetabolismMalabsorption SyndromesMiceModels, TheoreticalLeukocyte L1 Antigen ComplexLipidsenvironmental enteric dysfunctionlipid malabsorptionlow-grade inflammationsmall intestinestunted child growth

Identifiers

PMID36197997
PMCPMC9573096
OpenAlexW4302027591

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.