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.