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Solobacterium moorei promotes the progression of adenomatous polyps by causing inflammation and disrupting the
Shoujuan Yu1, Xifan Wang2, Ziyang Li3
1College of Food Science and Nutritional Engineering, China Agricultural University, Beijing, 100083, China.
Background:
Adenomatous polyps (APs) with inflammation are risk factors for colorectal cancer. However, the role of inflammation-related gut microbiota in promoting the progression of APs is unknown.
Methods:
Sequencing of the 16S rRNA gene was conducted to identify characteristic bacteria in AP tissues and normal mucosa. Then, the roles of inflammation-related bacteria were clarified by Spearman correlation analysis. Furthermore, colorectal HT-29 cells, normal colon NCM460 cells, and azoxymethane-treated mice were used to investigate the effects of the characteristic bacteria on progression of APs.
Results:
The expression levels of inflammation-related markers (diamine oxidase, D-lactate, C-reactive protein, tumor necrosis factor-α, interleukin-6 and interleukin-1β) were increased, whereas the expression levels of anti-inflammatory factors (interleukin-4 and interleukin-10) were significantly decreased in AP patients as compared to healthy controls. Solobacterium moorei (S. moorei) was enriched in AP tissues and fecal samples, and significantly positively correlated with serum inflammation-related markers. In vitro, S. moorei preferentially attached to HT-29 cells and stimulated cell proliferation and production of pro-inflammatory factors. In vivo, the incidence of intestinal dysplasia was significantly increased in the S. moorei group. Gavage of mice with S. moorei upregulated production of pro-inflammatory factors, suppressed proliferation of CD4+ and CD8+cells, and disrupted the integrity of the intestinal barrier, thereby accelerating progression of APs.
Conclusions:
S. moorei accelerated the progression of AP in mice via activation of the NF-κB signaling pathway, chronic low-grade inflammation, and intestinal barrier disruption. Targeted reduction of S. moorei presents a potential strategy to prevent the progression of APs.
Insights
Solobacterium moorei accelerates adenomatous polyp progression by increasing inflammation and disrupting the gut barrier. Reducing this bacterium may help prevent polyp development.
Area of Science:
- Gastroenterology
- Microbiology
- Oncology
Background:
- Adenomatous polyps (APs) with inflammation are risk factors for colorectal cancer.
- The role of inflammation-related gut microbiota in AP progression is unclear.
Purpose of the Study:
- To investigate the role of inflammation-related gut microbiota in the progression of adenomatous polyps.
- To identify specific bacteria associated with APs and their mechanisms of action.
Main Methods:
- 16S rRNA gene sequencing to identify bacteria in AP tissues and normal mucosa.
- Spearman correlation analysis to link bacteria with inflammation markers.
- In vitro and in vivo studies using cell lines and mouse models to assess bacterial effects on AP progression.
Main Results:
- Solobacterium moorei (S. moorei) was enriched in AP tissues and correlated with inflammation markers.
- S. moorei promoted HT-29 cell proliferation and pro-inflammatory cytokine production in vitro.
- In vivo, S. moorei accelerated intestinal dysplasia, increased pro-inflammatory factors, and disrupted the intestinal barrier in mice.
Conclusions:
- S. moorei accelerates AP progression through NF-κB activation, chronic inflammation, and intestinal barrier disruption.
- Targeted reduction of S. moorei shows potential for preventing AP progression.
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