Gut Liver.
2022 Jul;16(4):575-588. 10.5009/gnl210177.
Gut Microbiota Alteration Influences Colorectal Cancer Metastasis to the Liver by Remodeling the Liver Immune Microenvironment
- Affiliations
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- 1Department of Oncology, Hebei Medical University, Shijiazhuang, China.
- 2The Third Department of Oncology, Hebei General Hospital, Shijiazhuang, China.
- 3Department of Radiotherapy, The First Affiliated Hospital of Hebei North University, Zhangjiakou, China.
- 4Department of Clinical Psychology, Baoding No.1 Central Hospital, Baoding, China.
- 5Department of Thoracic Surgery, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
- 6Department of Oncology, Affiliated Hospital of Hebei University, Baoding, China.
- 7Department of General Surgery, The First Hospital of Hebei Medical University, Shijiazhuang, China.
- KMID: 2531240
- DOI: http://doi.org/10.5009/gnl210177
Abstract
- Background/Aims
This study aimed to explore the effect of gut microbiota-regulated Kupffer cells (KCs) on colorectal cancer (CRC) liver metastasis.
Methods
A series of in vivo and in vitro researches were showed to demonstrate the gut microbiota and its possible mechanism in CRC liver metastasis.
Results
Fewer liver metastases were identified in the ampicillin-streptomycin-colistin and colistin groups. Increased proportions of Parabacteroides goldsteinii, Bacteroides vulgatus, Bacteroides thetaiotaomicron, and Bacteroides uniforms were observed in the colistin group. The significant expansion of KCs was identified in the ampicillin-streptomycin-colistin and colistin groups. B.vulgatus levels were positively correlated with KC levels. More liver metastases were observed in the vancomycin group. An increased abundance of Parabacteroides distasonis and Proteus mirabilis and an obvious reduction of KCs were noted in the vancomycin group. P. mirabilis levels were negatively related to KC levels. The number of liver metastatic nodules was increased in the P. mirabilis group and decreased in the B. vulgatus group. The number of KCs decreased in the P. mirabilis group and increased in the B. vulgatus group. In vitro, as P. mirabilis or B. vulgatus doses increased, there was an opposite effect on KC proliferation in dose- and time-dependent manners. P. mirabilis induced CT26 cell migration by controlling KC proliferation, whereas B. vulgatus prevented this migration.
Conclusions
An increased abundance of P. mirabilis and decreased amount of B. vulgatus play key roles in CRC liver metastasis, which might be related to KC reductions in the liver.
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