AI Article Synopsis

  • This study investigates how gut microbiota influences the function of Kupffer cells (KCs) and their role in colorectal cancer (CRC) liver metastasis.
  • Results showed that certain antibiotic treatments (ampicillin-streptomycin-colistin) led to fewer liver metastases and an increase in the number of KCs, while vancomycin treatment resulted in more metastases and fewer KCs.
  • The findings suggest that the balance of gut bacteria and KCs may significantly affect the spread of CRC to the liver, with more KCs potentially helping to limit metastasis.

Article 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 and 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 , , , and were observed in the colistin group. The significant expansion of KCs was identified in the ampicillin-streptomycin-colistin and colistin groups. levels were positively correlated with KC levels. More liver metastases were observed in the vancomycin group. An increased abundance of and Proteus mirabilis and an obvious reduction of KCs were noted in the vancomycin group. levels were negatively related to KC levels. The number of liver metastatic nodules was increased in the group and decreased in the group. The number of KCs decreased in the group and increased in the group. In vitro, as or doses increased, there was an opposite effect on KC proliferation in dose- and time-dependent manners. induced CT26 cell migration by controlling KC proliferation, whereas prevented this migration.

Conclusions: An increased abundance of and decreased amount of play key roles in CRC liver metastasis, which might be related to KC reductions in the liver.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9289841PMC
http://dx.doi.org/10.5009/gnl210177DOI Listing

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