Evidence map›Paper›PMID 33154424›Full record

ArticleScientific reports2020

Butyrate induced Tregs are capable of migration from the GALT to the pancreas to restore immunological tolerance during type-1 diabetes.

Neenu Jacob, Shivani Jaiswal, Deep Maheshwari, Nayudu Nallabelli, Neeraj Khatri, Alka Bhatia, Amanjit Bal, Vivek Malik, Savita Verma, Rakesh Kumar and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

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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

11 authors at 2 institutions in 1 country.

Neenu JacobDepartment of Pediatrics, Post Graduate Institute of Medical Education and Research (PGIMER), Chandigarh, India.
Shivani JaiswalDepartment of Endocrinology, Post Graduate Institute of Medical Education and Research (PGIMER), Chandigarh, India.
Deep MaheshwariDepartment of Endocrinology, Post Graduate Institute of Medical Education and Research (PGIMER), Chandigarh, India.
Nayudu NallabelliDepartment of Endocrinology, Post Graduate Institute of Medical Education and Research (PGIMER), Chandigarh, India.
Neeraj KhatriiCARE, Institute of Microbial Technology (IMTech), Chandigarh, India.
Alka BhatiaDepartment of Experimental Medicine and Biotechnology, Post Graduate Institute of Medical Education and Research (PGIMER), Chandigarh, India.
Amanjit BalDepartment of Histopathology, Post Graduate Institute of Medical Education and Research (PGIMER), Chandigarh, India.
Vivek MalikSchool of Public Health, Post Graduate Institute of Medical Education and Research (PGIMER), Chandigarh, India.
Savita VermaDepartment of Pediatrics, Post Graduate Institute of Medical Education and Research (PGIMER), Chandigarh, India.
Rakesh KumarDepartment of Pediatrics, Post Graduate Institute of Medical Education and Research (PGIMER), Chandigarh, India.
Naresh SachdevaDepartment of Endocrinology, Post Graduate Institute of Medical Education and Research (PGIMER), Chandigarh, India. naresh_pgi@hotmail.com.
Post Graduate Institute of Medical Education and Research · INInstitute of Microbial Technology · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type-1 diabetes (T1D) is an autoimmune disease caused by progressive loss of insulin-producing beta cells in the pancreas. Butyrate is a commensal microbial-derived metabolite, implicated in intestinal homeostasis and immune regulation. Here, we investigated the mechanism of diabetes remission in non-obese diabetic (NOD) mice following butyrate administration. Sodium butyrate (150 mM) was administered to female NOD mice in drinking water after the onset of hyperglycemia (15-25 weeks age) and at 4 weeks of age (early-intervention group). Butyrate administration reduced the progression of hyperglycemia in diabetic mice and delayed onset of diabetes in the early-intervention group with a reduction in insulitis. Butyrate administration increased regulatory T cells (Tregs) in the colon, mesenteric lymph nodes, Peyer's patches, and its protective effects diminished upon depletion of Tregs. Further, an increase in α4β7, CCR9, and GPR15 expressing Tregs in the pancreatic lymph nodes (PLN) and pancreas in butyrate-treated mice suggested migration of gut-primed Tregs towards the pancreas. Finally, the adoptive transfer experiments demonstrated that induced Tregs from gut-associated lymphoid tissue can migrate towards the pancreas and PLN and delay the onset of diabetes. Our results thus suggest that early administration of butyrate can restore immunological tolerance during T1D via induction of Tregs with migratory capabilities.

Indexed as

AnimalsButyric AcidCell MovementDiabetes Mellitus, Type 1Disease ProgressionFemaleImmune ToleranceLymphoid TissueMiceMice, Inbred NODPancreasT-Lymphocytes, RegulatoryButyric Acid

Identifiers

PMID33154424
PMCPMC7644709
OpenAlexW3096212954

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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.