Skip to main content

ORIGINAL RESEARCH article

Front. Microbiol.
Sec. Microorganisms in Vertebrate Digestive Systems
Volume 16 - 2025 | doi: 10.3389/fmicb.2025.1541800

The gastric microbiome altered by A4GNT deficiency in mice

Provisionally accepted
Dawei Gong Dawei Gong 1,2Yuqiang Gao Yuqiang Gao 3*Rui Shi Rui Shi 4*Xiaona Xu Xiaona Xu 5*Mengchao Yu Mengchao Yu 5Shumin Zhang Shumin Zhang 1*Lili Wang Lili Wang 5*Quanjiang Dong Quanjiang Dong 5*
  • 1 Fourth People’s Hospital of Jinan, Jinan, Shandong Province, China
  • 2 Central Laboratories, the affiliated Qingdao Municipal Hospital of Dalian Medical University, Central Laboratories, the affiliated Qingdao Municipal Hospital of Dalian Medical University, China
  • 3 Department of Gastroenterology, Qingdao Municipal Hospital, Central Laboratories and Department of Gastroenterology, Qingdao Municipal Hospital, China
  • 4 Qingdao University Medical College, Qingdao, Shandong Province, China
  • 5 Central Laboratories, Qingdao Municipal Hospital, Central Laboratories and Department of Gastroenterology, Qingdao Municipal Hospital, China

The final, formatted version of the article will be published soon.

    Background: Selective antimicrobial effects have been found for α1,4-linked N-acetylglucosamine residues at the terminus of O-glycans attached to a core protein of gastric gland mucin. A4gnt encodes α1,4-N-acetylglucosaminyl transferase, which is responsible for the biosynthesis of α1,4-linked N-acetylglucosamine. The impact of A4GNT on the establishment and homeostasis of the gastric microbiome remains to be clarified. The aim of this study was to characterize the gastric microbiome in mice deficient for the production of α1,4-linked N-acetylglucosamine.The gastric microbiome within A4gnt -/-mice and wild-type mice was analyzed using high-throughput sequencing of bacterial 16S rRNA.Results: In A4gnt -/-mice, which spontaneously develop gastric cancer, the community structure of the gastric microbiome was altered. The relative abundance of mutagenic Desulfovibrio and proinflammatory Prevotellamassilia in these mice was significantly increased, especially 4 weeks after birth. The co-occurrence network appeared to be much more complex. Functional prediction demonstrated considerable decreases in the relative frequencies of functions associated with polysaccharide metabolism and transportation.The distinct profile in A4gnt -/-mice demonstrated a vital role of A4GNT in the establishment of the gastric microbiome. A dysbiotic gastric microbiome may contribute to the spontaneous development of gastric cancer in mice.

    Keywords: A4gnt, Gastric microbiome, Desulfovibrio, Prevotellamassilia, gastric cancer

    Received: 08 Dec 2024; Accepted: 24 Jan 2025.

    Copyright: © 2025 Gong, Gao, Shi, Xu, Yu, Zhang, Wang and Dong. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Yuqiang Gao, Department of Gastroenterology, Qingdao Municipal Hospital, Central Laboratories and Department of Gastroenterology, Qingdao Municipal Hospital, China
    Rui Shi, Qingdao University Medical College, Qingdao, Shandong Province, China
    Xiaona Xu, Central Laboratories, Qingdao Municipal Hospital, Central Laboratories and Department of Gastroenterology, Qingdao Municipal Hospital, China
    Shumin Zhang, Fourth People’s Hospital of Jinan, Jinan, Shandong Province, China
    Lili Wang, Central Laboratories, Qingdao Municipal Hospital, Central Laboratories and Department of Gastroenterology, Qingdao Municipal Hospital, China
    Quanjiang Dong, Central Laboratories, Qingdao Municipal Hospital, Central Laboratories and Department of Gastroenterology, Qingdao Municipal Hospital, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.