Evidence map›Paper›PMID 28667430›Full record

ArticleDigestive diseases and sciences2017

Attenuated GABAergic Signaling in Intestinal Epithelium Contributes to Pathogenesis of Ulcerative Colitis.

Surbhi Aggarwal, Vineet Ahuja, Jaishree Paul

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Article in Digestive diseases and sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
0.9field-weighted citation impact, top 31% 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

26 citing papers in PubMed, 36 citations in OpenAlex.

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  10. Experimental colitis-induced visceral hypersensitivity is attenuated by GABA treatment in mice.American journal of physiology. Gastrointestinal and liver physiology · 2024
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  14. Inhibition of GABAInternational journal of molecular sciences · 2022
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  18. Neuroimmunomodulation by gut bacteria: Focus on inflammatory bowel diseases.World journal of gastrointestinal pathophysiology · 2021
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Surbhi AggarwalSchool of Life Sciences, Jawaharlal Nehru University, New Delhi, 110067, India.
Vineet AhujaDepartment of Gastroenterology, All India Institute of Medical Sciences, New Delhi, 110067, India.
Jaishree PaulSchool of Life Sciences, Jawaharlal Nehru University, New Delhi, 110067, India. jpaul33@hotmail.com.
Jawaharlal Nehru University · INAll India Institute of Medical Sciences · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeuromediators produced by enteric nervous system regulate inflammatory processes via interacting with enteric immune system. Role of γ-aminobutyric acid (GABA), which is also a neuromediator, has been implicated in autoimmune diseases like multiple sclerosis, type 1 diabetes, and rheumatoid arthritis, where they modulate the immune responses. However, its role in ulcerative colitis (UC) has not been defined.

aimsThis study was carried out to investigate the role of GABA and its signaling components in pathogenesis of UC.

methodsPeripheral blood, colon mucosal biopsy, and fecal specimens were collected from UC and control groups. Quantification of GABA was done using ELISA. Expression of GABAergic signal system components was analyzed through RT-PCR analysis. Enumeration of GABA-producing bacteria was done by qPCR analysis. Activity of p38 MAPK and expression of proinflammatory cytokines were determined by immunohistochemistry and RT-PCR analysis, respectively.

resultsGABA levels were significantly reduced in patients with UC as compared to control group when measured in serum and colon biopsy. Altered expression of GABAergic signal system was observed in UC patients. Reduced abundance of selected GABA-producing bacteria was detected in stool samples of UC patients as compared to control. p38 MAPK activity and expression of its downstream effector cytokines were found to be increased in UC patients as compared to control.

conclusionsReduced levels of GABA were observed in patients with UC, and this leads to hyperactivation of p38 MAPK and overexpression of downstream effector cytokines suggesting a role of GABA in pathogenesis of UC.

Indexed as

AdultBacteriaBiopsyCase-Control StudiesColitis, UlcerativeColonCytokinesDown-RegulationFecesFemalegamma-Aminobutyric AcidHumansInflammation MediatorsIntestinal MucosaMaleMiddle AgedCytokinesgamma-Aminobutyric AcidInflammation Mediatorsp38 Mitogen-Activated Protein KinasesReceptors, GABACytokinesEnteric nervous systemGABAGABA receptorInflammationNeurotransmitterp38 MAPKUlcerative colitis

Identifiers

PMID28667430
OpenAlexW2731399089

What OpenQuestion holds

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Registered trials

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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.