Evidence map›Paper›PMID 30930024›Full record

ArticleGastroenterology2019

Interactions Between Commensal Bacteria and Enteric Neurons, via FPR1 Induction of ROS, Increase Gastrointestinal Motility in Mice.

Bindu Chandrasekharan, Bejan J Saeedi, Ashfaqul Alam, Madelyn Houser, Shanthi Srinivasan, Malu Tansey, Rheinallt Jones, Asma Nusrat, Andrew S Neish

Open access · greenAbstract read
In one paragraph

Article in Gastroenterology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.

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  19. Microbiota-derived acetylcholine can promote gut motility inPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024
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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

9 authors at 2 institutions in 1 country.

Bindu ChandrasekharanDepartment of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia.
Bejan J SaeediDepartment of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia.
Ashfaqul AlamDepartment of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia.
Madelyn HouserDepartment of Physiology, Emory University, Atlanta, Georgia.
Shanthi SrinivasanDepartment of Medicine (Digestive Diseases), Emory University, Atlanta, Georgia; VA Medical Centre, Decatur, Georgia.
Malu TanseyDepartment of Physiology, Emory University, Atlanta, Georgia.
Rheinallt JonesDepartment of Pediatrics, Emory University, Atlanta, Georgia.
Asma NusratDepartment of Pathology and Laboratory Medicine, University of Michigan, Ann Arbor Michigan.
Andrew S NeishDepartment of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia. Electronic address: aneish@emory.edu.
Emory University · USUniversity of Michigan · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM008169 · NIGMS · EMORY UNIVERSITY · PI GROSS, ROBERT E · 1987 to 2021
$20.3M
Mechanism of Enteric NeuropathyR01DK080684 · NIDDK · EMORY UNIVERSITY · PI Shanthi K Srinivasan · 2009 to 2026
$6.1M
Microbial Influence on Mucosal HomeostasisR01AI064462 · NIAID · EMORY UNIVERSITY · PI NEISH, ANDREW S · 2006 to 2022
$5.5M
Formyl peptide receptors as mediators of intestinal mucosal homeostasisR01DK089763 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NEISH, ANDREW S, NUSRAT, ASMA · 2011 to 2020
$4.7M
Formyl peptide receptors as mediators of intestinal mucosal homeostasisR56DK089763 · NIDDK · EMORY UNIVERSITY · PI NEISH, ANDREW S, NUSRAT, ASMA · 2010 to 2010
$741k
Microbially generated protons mediate interkingdom host-microbiome cross-talk and maintain intestinal homeostasis via reciprocal functions of two proton-sensing GPCRsK01DK114391 · NIDDK · UNIVERSITY OF KENTUCKY · PI ALAM, M. ASHFAQUL · 2017 to 2021
$530k
Epithelial specific ubiquitination eventsR56AI064462 · NIAID · EMORY UNIVERSITY · PI NEISH, ANDREW S · 2011 to 2011
$379k
BLRD VA I01 BX000136NIAID NIH HHS R01 AI064462NIAID NIH HHS R56 AI064462NIDDK NIH HHS K01 DK114391NIDDK NIH HHS R01 DK080684NIDDK NIH HHS R01 DK089763NIDDK NIH HHS R56 DK089763NIGMS NIH HHS T32 GM008169
6 · The paper itself

Abstract

BACKGROUND &

aimsReduced gastrointestinal (GI) motility is a feature of disorders associated with intestinal dysbiosis and loss of beneficial microbes. It is not clear how consumption of beneficial commensal microbes, marketed as probiotics, affects the enteric nervous system (ENS). We studied the effects of the widely used probiotic and the commensal Lactobacillus rhamnosus GG (LGG) on ENS and GI motility in mice.

methodsConventional and germ free C57B6 mice were gavaged with LGG and intestinal tissues were collected; changes in the enteric neuronal subtypes were assessed by real-time polymerase chain reaction, immunoblots, and immunostaining. Production of reactive oxygen species (ROS) in the jejunal myenteric plexi and phosphorylation (p) of mitogen-activated protein kinase 1 (MAPK1) in the enteric ganglia were assessed by immunoblots and immunostaining. Fluorescence in situ hybridization was performed on jejunal cryosections with probes to detect formyl peptide receptor 1 (FPR1). GI motility in conventional mice was assessed after daily gavage of LGG for 1 week.

resultsFeeding of LGG to mice stimulated myenteric production of ROS, increased levels of phosphorylated MAPK1, and increased expression of choline acetyl transferase by neurons (P < .001). These effects were not observed in mice given N-acetyl cysteine (a ROS inhibitor) or LGGΩSpaC (an adhesion-mutant strain of LGG) or FPR1-knockout mice. Gavage of mice with LGG for 1 week significantly increased stool frequency, reduced total GI transit time, and increased contractions of ileal circular muscle strips in ex vivo experiments (P < .05).

conclusionsUsing mouse models, we found that LGG-mediated signaling in the ENS requires bacterial adhesion, redox mechanisms, and FPR1. This pathway might be activated to increase GI motility in patients.

Indexed as

Lacticaseibacillus rhamnosusProbioticsAcetylcysteineAnimalsAntioxidantsCholine O-AcetyltransferaseEnteric Nervous SystemGastrointestinal MotilityGastrointestinal TransitGerm-Free LifeIleumIn Situ Hybridization, FluorescenceJejunumMiceMice, KnockoutMitogen-Activated Protein Kinase 1AcetylcysteineAntioxidantsCholine O-AcetyltransferaseFpr1 protein, mouseMapk1 protein, mouseMitogen-Activated Protein Kinase 1Reactive Oxygen SpeciesReceptors, Formyl PeptideDigestionERKMicrobiomeSignal Transduction

Identifiers

PMID30930024
PMCPMC8733963
OpenAlexW2929891454

What OpenQuestion holds

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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.