Evidence map›Paper›PMID 39277690›Full record

ArticleCommunications biology2024

Contribution of collagen-binding protein Cnm of Streptococcus mutans to induced IgA nephropathy-like nephritis in rats.

Shuhei Naka, Daiki Matsuoka, Taro Misaki, Yasuyuki Nagasawa, Seigo Ito, Ryota Nomura, Kazuhiko Nakano, Michiyo Matsumoto-Nakano

Abstract read
In one paragraph

Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Binding of IgA1 and surface-expressed collagen-binding protein ofFrontiers in cellular and infection microbiology · 2025
    Article
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

8 authors.

Shuhei Naka *Department of Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan.
Daiki Matsuoka *Department of Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan.
Taro MisakiDivision of Nephrology, Seirei Hamamatsu General Hospital, Hamamatsu, Shizuoka, Japan.
Yasuyuki NagasawaDepartment of General Internal Medicine, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan.
Seigo ItoDepartment of Internal Medicine, Japan Self-Defense Force Iruma Hospital, Saitama, Japan.
Ryota NomuraDepartment of Pediatric Dentistry, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Kazuhiko NakanoDepartment of Pediatric Dentistry, Graduate School of Dentistry, The University of Osaka, Suita, Osaka, Japan.ORCID 0000-0002-2209-2685
Michiyo Matsumoto-NakanoDepartment of Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan. mnakano@okayama-u.ac.jp.ORCID 0009-0007-8650-0477

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IgA nephropathy (IgAN), the most common primary glomerulonephritis, is considered an intractable disease with unknown pathogenic factors. In our previous study, Streptococcus mutans, the major causative bacteria of dental caries, which expresses Cnm, was related to the induction of IgAN-like nephritis. In the present study, the Cnm-positive S. mutans parental strain, a Cnm-defective isogenic mutant strain, its complementation strain, and recombinant Cnm (rCnm) protein were administered intravenously to Sprague Dawley rats, and the condition of their kidneys was evaluated focusing on the pathogenicity of Cnm. Rats treated with parental and complement bacterial strains and rCnm protein developed IgAN-like nephritis with mesangial proliferation and IgA and C3 mesangial deposition. Scanning immunoelectron microscopy revealed that rCnm was present in the electron-dense deposition area of the mesangial region in the rCnm protein group. These results demonstrated that the Cnm protein itself is an important factor in the induction of IgAN in rats.

Indexed as

Adhesins, BacterialGlomerulonephritis, IGAStreptococcus mutansAnimalsCarrier ProteinsDisease Models, AnimalMaleRatsRats, Sprague-DawleyAdhesins, BacterialCarrier ProteinsCnm protein, Streptococcus mutans

Identifiers

PMID39277690
PMCPMC11401903

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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.