Evidence map›Paper›PMID 36693853›Full record

ArticleCell death discovery2023

Gut microbiota and microbiota-derived metabolites promotes endometriosis.

Sangappa B Chadchan, Sumanta K Naik, Pooja Popli, Chandni Talwar, Satwikreddy Putluri, Chandrasekhar R Ambati, Michael A Lint, Andrew L Kau, Christina L Stallings, Ramakrishna Kommagani

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 2 pooled it
20.2field-weighted citation impact, top 1% 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

65 citing papers in PubMed, 2 syntheses or guidelines pooled it, 74 citations in OpenAlex.

  1. Pooled it
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  3. Microbiome and chronic pelvic pain in women: a mini-review.Human reproduction (Oxford, England) · 2026
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5 more citing papers are in PubMed but not listed here.

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

10 authors at 2 institutions in 1 country.

Sangappa B ChadchanDepartment of Pathology and Immunology, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030, USA.
Sumanta K NaikDepartment of Molecular Microbiology, Washington University School of Medicine, St. Louis, MO, 63110, USA.ORCID http://orcid.org/0000-0003-4499-0811
Pooja PopliDepartment of Pathology and Immunology, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030, USA.
Chandni TalwarDepartment of Pathology and Immunology, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030, USA.
Satwikreddy PutluriDepartment of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030, USA.
Chandrasekhar R AmbatiAdvanced Technology Core, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030, USA.
Michael A LintCenter for Women's Infectious Disease Research, Washington University School of Medicine, St. Louis, MO, 63110, USA.
Andrew L KauCenter for Women's Infectious Disease Research, Washington University School of Medicine, St. Louis, MO, 63110, USA.
Christina L StallingsDepartment of Molecular Microbiology, Washington University School of Medicine, St. Louis, MO, 63110, USA.
Ramakrishna KommaganiDepartment of Pathology and Immunology, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030, USA. rama.kommagani@bcm.edu.ORCID http://orcid.org/0000-0003-0403-0971
Baylor College of Medicine · USWashington University in St. Louis · US

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI Michael M Ittmann · 2007 to 2026
$73.9M
MOLECULAR AND METABOLIC ASPECTS OF IMPLANTATIONR01HD065435 · NICHD · WASHINGTON UNIVERSITY · PI KOMMAGANI, RAMAKRISHNA, SANTI, CELIA M · 2010 to 2020
$4.5M
ROLE OF THE GUT MICROBIOTA IN ENDOMETRIOSISR01HD102680 · NICHD · WASHINGTON UNIVERSITY · PI Ramakrishna Kommagani · 2021 to 2026
$2.4M
Identify the DNA Adduct and Associated Metabolic Alterations in Bladder Cancer of SmokersR01CA216426 · NCI · BAYLOR COLLEGE OF MEDICINE · PI EL-ZEIN, RANDA A, PUTLURI, NAGIREDDY · 2018 to 2022
$2.0M
Racial Disparity in Bladder Cancer and Identification of Altered Metabolism in African American Compare to European Bladder CancerR01CA220297 · NCI · BAYLOR COLLEGE OF MEDICINE · PI PUTLURI, NAGIREDDY · 2017 to 2021
$1.8M
GREB1 Action in Endometrial Function and DysfunctionR00HD080742 · NICHD · WASHINGTON UNIVERSITY · PI KOMMAGANI, RAMAKRISHNA · 2017 to 2019
$702k
NCI NIH HHS P30 CA125123NCI NIH HHS R01 CA216426NCI NIH HHS R01 CA220297NICHD NIH HHS R00 HD080742NICHD NIH HHS R01 HD065435NICHD NIH HHS R01 HD102680
6 · The paper itself

Abstract

Endometriosis is a pathological condition of the female reproductive tract characterized by the existence of endometrium-like tissue at ectopic sites, affecting 10% of women between the age 15 and 49 in the USA. However, currently there is no reliable non-invasive method to detect the presence of endometriosis without surgery and many women find hormonal therapy and surgery as ineffective in avoiding the recurrences. There is a lack of knowledge on the etiology and the factors that contribute to the development of endometriosis. A growing body of recent evidence suggests an association between gut microbiota and endometriosis pathophysiology. However, the direct impact of microbiota and microbiota-derived metabolites on the endometriosis disease progression is largely unknown. To understand the causal role of gut microbiota and endometriosis, we have implemented a novel model using antibiotic-induced microbiota-depleted (MD) mice to investigate the endometriosis disease progression. Interestingly, we found that MD mice showed reduced endometriotic lesion growth and, the transplantation of gut microbiota by oral gavage of feces from mice with endometriosis rescued the endometriotic lesion growth. Additionally, using germ-free donor mice, we indicated that the uterine microbiota is dispensable for endometriotic lesion growth in mice. Furthermore, we showed that gut microbiota modulates immune cell populations in the peritoneum of lesions-bearing mice. Finally, we found a novel signature of microbiota-derived metabolites that were significantly altered in feces of mice with endometriosis. Finally, we found one the altered metabolite, quinic acid promoted the survival of endometriotic epithelial cells in vitro and lesion growth in vivo, suggesting the disease-promoting potential of microbiota-derived metabolites. In summary, these data suggest that gut microbiota and microbiota-derived metabolome contribute to lesion growth in mice, possibly through immune cell adaptations. Of translational significance, these findings will aid in designing non-invasive diagnostics using stool metabolites for endometriosis.

Identifiers

PMID36693853
PMCPMC9873805
OpenAlexW4317889673

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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.