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Background Colorectal cancer (CRC) is a major cause of cancer mortality worldwide, with metastatic spread accounting for most CRC-related deaths. Recent studies have identified the presence of gut mycobiome across various cancer types including CRC. However, the contribution to CRC metastasis of intestinal fungi remains poorly defined.Methods Fecal samples from CRC patients were collected for ITS rDNA sequencing. Animal models of CRC metastasis (MC38 cell line, tail-vain injection) were used to explore the effect of Candida albicans in promoting tumor metastasis. Single-cell RNA sequencing was used to characterize changes in the immune microenvironment within metastatic lesions, which were validated by flow cytometry and multiplex immunofluorescence.Results CRC patients with distant metastases exhibited altered gut mycobiota, notably an enrichment of C. albicans. In CRC metastasis mouse models, oral administration of C. albicans and intraperitoneal injection of candidalysin enhanced metastatic burden, whereas this effect was attenuated using an ece1-deficient strain. ScRNA sequencing of lung immune cells revealed increased neutrophils with a neutrophil extracellular traps (NET) formation phenotype after C. albicans treatment. Our analyses demonstrated that the pro-metastatic effect of C. albicans is mediated by macrophage recruitment of neutrophils via the CCL6-CCR1 signaling axis. Depletion of either macrophages or neutrophils attenuates this metastatic promotion. Candidalysin enhanced neutrophil migration in a macrophage–neutrophil co-culture experiment. Using macrophage-specific CARD9 knockout mice and macrophage depletion followed by adoptive transfer experiments, we confirmed that the observed phenotype was mediated via the CARD9 signaling pathway in macrophages. Transcriptomic sequencing revealed that Candidalysin activates NF-κB via Card9 in macrophages, which in turn upregulates CCL6 expression. Disruption of the macrophage-neutrophil axis—through NET degradation (DNaseI) or CCR1 antagonism—reduced the pro-metastatic effect of C. albicans.Conclusions CRC patients with distant metastases have significantly elevated intestinal colonization by C. albicans compared to non-metastatic cases. Mechanistically, C. albicans-derived candidalysin activates macrophage CARD9–NF-κB signaling, leading to robust upregulation of the chemokine CCL6. The increased CCL6 levels recruit neutrophils to the lung and enhance NET formation, creating a pro-metastatic niche for colorectal tumor cells.