Evidence map›Paper›PMID 39910460›Full record

ArticleBMC gastroenterology2025

Helicobacter pylori CagA+ strains modulate colorectal pathology by regulating intestinal flora.

Shasha Cui, Xinqiang Liu, Fengxia Han, Lu Zhang, Jingjing Bu, Sainan Wu, Jiafen Wang

Abstract read
In one paragraph

Article in BMC gastroenterology, 2025. 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. Review
  2. Article
  3. Article
  4. Article
  5. A critical review onFrontiers in cellular and infection microbiology · 2025
    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

7 authors.

Shasha CuiClinical Laboratory, Binzhou People's Hospital, No.515, Huangheqi Road, Bincheng District, Binzhou, Shandong Province, 256610, P. R. China.
Xinqiang LiuDepartment of Oncology, Binzhou People's Hospital, Binzhou, Shandong Province, 256610, P. R. China.
Fengxia HanClinical Laboratory, Binzhou People's Hospital, No.515, Huangheqi Road, Bincheng District, Binzhou, Shandong Province, 256610, P. R. China.
Lu ZhangDepartment of Oncology, Binzhou People's Hospital, Binzhou, Shandong Province, 256610, P. R. China.
Jingjing BuClinical Laboratory, Binzhou People's Hospital, No.515, Huangheqi Road, Bincheng District, Binzhou, Shandong Province, 256610, P. R. China.
Sainan WuClinical Laboratory, Binzhou People's Hospital, No.515, Huangheqi Road, Bincheng District, Binzhou, Shandong Province, 256610, P. R. China.
Jiafen WangClinical Laboratory, Binzhou People's Hospital, No.515, Huangheqi Road, Bincheng District, Binzhou, Shandong Province, 256610, P. R. China. wjf2020wjf@126.com.

Funding

Project of Binzhou People's Hospital LCYJZR202116
6 · The paper itself

Abstract

aimThis article aims to investigate the role of Helicobacter Pylori (HP) CagA+ strains affected colorectal lesion via gut microbiota.

method6-week C57BL/6J mice were divided into: (a) HP CagA+ group undergoing HP CagA+ strains administration by gavage at 0.2 mL for 10 days; (b) HP CagA- group undergoing HP CagA- strains administration by gavage at 0.2 mL for 10 days; (c) control group intragastrically given 0.2 mL of brian heart infusion (BHI) medium for 10 days. Gastric mucosa was collected for Giemsa staining, and colorectal mucosa was for hematoxylin and eosin (H&E) staining, 16 S ribosomal RNA (rRNA) sequencing and immunohistochemistry for Major Histocompatibility Complex (MHC). Colon tissues and serum from caudal vein was collected for quantification of interleukin (IL)-6, IL-8, IL10 and tumor necrosis factor (TNF-α).

resultsMice with HP CagA+ infection developed loss of some resident cells and inflammation infiltration in colorectal mucosa, and increased Giemsa-positive cells in gastric tissue. Also, MHC II-positive cells were increased in colorectal tissue in HP CagA+ strains infection. HP CagA+ infection cause increase of TNF-α, IL-6, IL-8 and IL-10 in the serum. Meanwhile, HP CagA+ stainis evoked gut microbiota dysbiosis which was characterized by altered microbiome distribution, reduction in Front-to-Back (F/B ratio), decreased α-diversity metric (Chao1 and Shannon). In β-diversity, gut microbiota in control and HP CagA+ groups showed the significant distance based on UniFrac distance. Cag group was enriched a higher abundance of Staphylococcus and Corynebacterium, while control subjects were enriched in Marinifilaceae and Odoribacter.

conclusionHP CagA+ strains are capable of causing gut microbiota dysbiosis to develop destruction of intestinal barrier, and it may affect the development of colorectal cancer by increasing colonization of Staphylococcus and Corynebacterium.

Indexed as

Antigens, BacterialBacterial ProteinsColonGastrointestinal MicrobiomeHelicobacter InfectionsHelicobacter pyloriAnimalsGastric MucosaIntestinal MucosaMaleMiceMice, Inbred C57BLAntigens, BacterialBacterial ProteinscagA protein, Helicobacter pyloriCagA+Colorectal lesionGut microbiotaHelicobacter pylori

Identifiers

PMID39910460
PMCPMC11796129

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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.