Evidence map›Paper›PMID 33810172›Full record

ArticleInternational journal of molecular sciences2021

Formation of Autoimmune Lesions Is Independent of Antibiotic Treatment in NOD Mice.

Mami Sato, Rieko Arakaki, Hiroaki Tawara, Takaaki Tsunematsu, Naozumi Ishimaru

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 52% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Review
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

5 authors at 1 institution in 1 country.

Mami SatoDepartment of Oral Molecular Pathology, Graduate School of Biomedical Sciences, Tokushima University, Tokushima 7708504, Japan.
Rieko ArakakiDepartment of Oral Molecular Pathology, Graduate School of Biomedical Sciences, Tokushima University, Tokushima 7708504, Japan.
Hiroaki TawaraDepartment of Oral Molecular Pathology, Graduate School of Biomedical Sciences, Tokushima University, Tokushima 7708504, Japan.
Takaaki TsunematsuDepartment of Oral Molecular Pathology, Graduate School of Biomedical Sciences, Tokushima University, Tokushima 7708504, Japan.
Naozumi IshimaruDepartment of Oral Molecular Pathology, Graduate School of Biomedical Sciences, Tokushima University, Tokushima 7708504, Japan.
Tokushima University · JP

Funding

Japan Society for the Promotion of Science 18K19648
6 · The paper itself

Abstract

The relationship between autoimmunity and changes in intestinal microbiota is not yet fully understood. In this study, the role of intestinal microbiota in the onset and progression of autoimmune lesions in non-obese diabetic (NOD) mice was evaluated by administering antibiotics to alter their intestinal microenvironment. Flow cytometric analysis of spleen cells showed that antibiotic administration did not change the proportion or number of T and B cells in NOD mice, and pathological analysis demonstrated that autoimmune lesions in the salivary glands and in the pancreas were also not affected by antibiotic administration. These results suggest that the onset and progression of autoimmunity may be independent of enteral microbiota changes. Our findings may be useful for determining the appropriate use of antibiotics in patients with autoimmune diseases who are prescribed drugs to maintain systemic immune function.

Indexed as

AutoimmunityDisease SusceptibilityAnimalsAnti-Bacterial AgentsAutoimmune DiseasesCytokinesDisease Models, AnimalImmune SystemMiceMice, Inbred NODSialadenitisAnti-Bacterial AgentsCytokinesantibiotic treatmentautoimmune lesionNOD miceSjögren’s syndrometype 1 diabetes

Identifiers

PMID33810172
PMCPMC8005129
OpenAlexW3136824986

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.