Evidence map›Paper›PMID 38874761›Full record

ArticleJournal of gastroenterology2024

Mouse IgA modulates human gut microbiota with inflammatory bowel disease patients.

Keishu Takahashi, Naoki Morita, Ryutaro Tamano, Peng Gao, Noriho Iida, Akira Andoh, Hirotsugu Imaeda, Ken Kurokawa, Mayo Tsuboi, Yoku Hayakawa and 2 more

Abstract read
In one paragraph

Article in Journal of gastroenterology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

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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

12 authors.

Keishu Takahashi *Institute for Quantitative Biosciences, The University of Tokyo, Bunkyo-ku, Tokyo, Japan, Laboratory of Immunology and Infection Control.
Naoki Morita *Institute for Quantitative Biosciences, The University of Tokyo, Bunkyo-ku, Tokyo, Japan, Laboratory of Immunology and Infection Control.
Ryutaro TamanoInstitute for Quantitative Biosciences, The University of Tokyo, Bunkyo-ku, Tokyo, Japan, Laboratory of Immunology and Infection Control.
Peng GaoInstitute for Quantitative Biosciences, The University of Tokyo, Bunkyo-ku, Tokyo, Japan, Laboratory of Immunology and Infection Control.
Noriho IidaDepartment of Gastroenterology, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Ishikawa, Japan.
Akira AndohDepartment of Medicine, Shiga University of Medical Science, Otsu, Shiga, Japan.
Hirotsugu ImaedaDepartment of Gastroenterology, Nagahama City Hospital, Nagahama, Shiga, Japan.
Ken KurokawaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Mayo TsuboiDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Yoku HayakawaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Mitsuhiro FujishiroDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Reiko ShinkuraInstitute for Quantitative Biosciences, The University of Tokyo, Bunkyo-ku, Tokyo, Japan, Laboratory of Immunology and Infection Control. rshinkura@iqb.u-tokyo.ac.jp.

Funding

AMED JP17gm1010008JST SPRING JPMJSP2108
6 · The paper itself

Abstract

backgroundThe imbalance of commensal bacteria is called dysbiosis in intestinal microflora. Secreted IgA in the intestinal lumen plays an important role in the regulation of microbiota. Although dysbiosis of gut bacteria is reported in IBD patients, it remains unclear what makes dysbiosis of their microflora. The intervention method for remedy of dysbiosis in IBD patients is not well established. In this study, we focused on the quality of human endogenous IgA and investigated whether mouse monoclonal IgA which binds to selectively colitogenic bacteria can modulate human gut microbiota with IBD patients.

methodsIgA-bound and -unbound bacteria were sorted by MACS and cell sorter. Sorted bacteria were analyzed by 16S rRNA sequencing to investigate what kinds of bacteria endogenous IgA or mouse IgA recognized in human gut microbiota. To evaluate the effect of mouse IgA, gnotobiotic mice with IBD patient microbiota were orally administrated with mouse IgA and analyzed gut microbiota.

resultsWe show that human endogenous IgA has abnormal binding activity to gut bacteria in IBD patients. Mouse IgA can bind to human microbiota and bind to selectively colitogenic bacteria. The rW27, especially, has a growth inhibitory activity to human colitogenic bacteria. Furthermore, oral administration of mouse IgA reduced an inflammation biomarker, fecal lipocalin 2, in mice colonized with IBD patient-derived microbiota, and improved dysbiosis of IBD patient sample.

conclusionOral treatment of mouse IgA can treat gut dysbiosis in IBD patients by modulating gut microbiota.

Indexed as

DysbiosisFecesGastrointestinal MicrobiomeImmunoglobulin AInflammatory Bowel DiseasesLipocalin-2AdultAnimalsFemaleGerm-Free LifeHumansMaleMiceMiddle AgedRNA, Ribosomal, 16SImmunoglobulin ALipocalin-2RNA, Ribosomal, 16SDysbiosisGut microbiotaIgAInflammatory bowel disease

Identifiers

PMID38874761
PMCPMC11339086

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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.