Objective：To investigate the role of microbes in colorectal cancer liver metastases(CRLM)and the underlying mechanisms. Methods：16S rDNA sequencing was performed on colon tumors and liver tumors in CRLM patients. The mouse model of CRLM was established and treated with antibiotics，Escherichia coli(E.coli)，lactate dehydrogenase inhibitor and clodronate liposome. After 24 days，the liver tumor tissues were obtained for HE staining，immunofluorescence staining and detection of lactate concentration and microbial abundance. E. coli and MC38 cells were co - cultured at 100∶1. The cell proliferation，the extracellular acidification rate(ECAR)and concentration of lactate was determined by CCK8，Seahorse and colorimetry respectively. Macrophages (MØ)derived from mouse bone marrow were treated with lactate，lactylation antibody and TNF-α respectively. The expression levels of CD206 and iNOS were detected by immunofluorescence；the mRNA levels of iNOS，CD86，CD163 and ARG were detected by qPCR； The lactylation level and NF-κB expression were detected by Western Blot. Results：There were microbes in colon and liver tumors in CRLM patients and the dominant species were similar. Microbiota promoted liver metastasis of colorectal cancer in mice and MØ was found to be M2 - like polarized，while the liver metastases decreased after depletion of MØ. Microbiota could not enhance the proliferation of tumor cells，but could increase the level of tumor glycolysis and lactate and inhibition of lactate dehydrogenase could reduce liver metastases in mice.Lactate could induce MØ polarization to M2 and lactylation. RIG - Ilys852 was found to inhibit the polarization of MØ induced by lactate;the expression of NF -κB was decreased after macrophage treated with lactate;TNF -α could inhibit MØ polarization to M2. Conclusion:Microbes enhance the level of glycolysis and lactate in tumor and promote liver metastasis of colorectal cancer via macrophage RIG-I lactylation.