Weizmannia coagulans BCF-01: a novel gastrogenic probiotic for Helicobacter pylori infection control

ABSTRACT

The widespread prevalence of Helicobacter pylori infection, particularly in China, contributes to the development of gastrointestinal diseases. Antibiotics have limitations, including adverse reactions and increased antibiotic resistance. Therefore, identification of novel gastrogenic probiotics capable of surviving the acidic gastric environment and effectively combating H. pylori infection has potential in restoring gastric microbiota homeostasis. Five novel strains of human gastrogenic Weizmannia coagulans (BCF-01–05) were isolated from healthy gastric mucosa and characterized using 16S rDNA identification. Acid resistance, H. pylori inhibition, and adherence to gastric epithelial cells were evaluated in in-vitro experiments and the molecular mechanism explored in in-vivo experiments. Among the gastric-derived W. coagulans strains, BCF-01 exhibited the strongest adhesion and H. pylori inhibition, warranting further in-vivo safety evaluation. Through 16S rRNA sequencing of a mouse model, BCF-01 was determined to significantly restore H. pylori-associated gastric dysbiosis and increase the abundance of potential probiotic bacteria. Furthermore, BCF-01 enhanced mucosal tight junction protein expression and inhibited the TLR4-NFκB-pyroptosis signaling pathway in macrophages, as demonstrated by qRT-PCR and western blotting.

These findings highlight the potential of BCF-01 in the prevention and control of H. pylori infection. Specifically, treatment with BCF-01 effectively restored gastric microecology and improved H. pylori-mediated mucosal barrier destruction while reducing inflammation through inhibition of the TLR4-NFκB-pyroptosis signaling pathway in macrophages. BCF-01 is a promising alternative to traditional triple therapy for H. pylori infections, offering minimal side effects with high suitability for high-risk individuals.

KEYWORDS:

• Human gastrogenic probiotic
• weizmannia coagulans BCF-01
• helicobacter pylori infection
• gastric microbiota homeostasis
• mucosal immunity

Acknowledgments

We would like to thank Editage (www.editage.cn) for English language editing. Figure 7 was created with Biorender (www.biorender.com, agreement number: NX26EOE2R5).

Disclosure statement

No potential conflict of interest was reported by the author(s).

Author contributions

Study design: Fan HY; Data collection: Chen ZH, Tang ZY, Li WD and Yang JX; Data analysis: Yu L, Huang WW, and Liu JX; Writing – Original Draft: Chen ZH; Visualization: Guo XT, Deng XS, Cheng YS, Zhou DX, and Shan JM. Writing – Review & Editing: Zeng WS and Bai Y;

Ethics approval and consent to participate

The patient signed a consent form for phage therapy, and for having research samples collected and processed, including microbiome analyses. This research was approved by the Ethics Committee of Nanfang Hospital, China (NFEC-2022-252).

Data availability statement

The data that support the findings of this study have been deposited in the CNGB Sequence Archive (CNSA) of the China National GeneBank DataBase (CNGBdb) under accession number CNP0005043.

Supplementary material

Supplemental data for this article can be accessed online at https://doi.org/10.1080/19490976.2024.2313770

Additional information

Funding

This work was supported by National Natural Science Foundation of China (No. 32300085, 32370139 & 32070118), the Clinical Research Project of Nanfang Hospital (No: 2021CR008), Key-Areas Research and Development Programs of Guangdong Province (No.2022B1111070006), Scientific Research Project of Administration of Traditional Chinese Medicine of Guangdong Province (No.20221269).