最近，在结直肠癌（CRC）患者中发现了肠道菌群失调，且口腔细菌丰富。在这里，我们表征并研究了其中一种口腔致病菌，即革兰氏阳性厌氧球菌微小单胞菌。我们确定了两种表现出不同表型和粘附能力的系统发育型（A 和 B）。我们观察到系统发育型 A 与 CRC 存在很强的相关性，与正常同源结肠粘膜相比，其在粪便和肿瘤组织中的丰度更高，这与患者独特的甲基化状态相关。通过开发人原代结肠细胞与厌氧菌的体外缺氧共培养系统，我们发现 P. micra 系统发育型 A 改变了关键肿瘤抑制基因、癌基因和参与上皮间质转化的基因的 DNA 甲基化谱启动子。在携带 P. micra 系统发育型 A 的 CRC 患者的结肠粘膜中，我们发现了类似的 DNA 甲基化改变，以及参与炎症、细胞粘附和肌动蛋白细胞骨架调节的通路中差异表达基因的显着富集，这为 P. micra 可能存在的证据提供了证据。在致癌过程中的作用。

Recently, an intestinal dysbiotic microbiota with enrichment in oral cavity bacteria has been described in colorectal cancer (CRC) patients. Here, we characterize and investigate one of these oral pathobionts, the Gram-positive anaerobic coccus Parvimonas micra. We identified two phylotypes (A and B) exhibiting different phenotypes and adhesion capabilities. We observed a strong association of phylotype A with CRC, with its higher abundance in feces and in tumoral tissue compared with the normal homologous colonic mucosa, which was associated with a distinct methylation status of patients. By developing an in vitro hypoxic co-culture system of human primary colonic cells with anaerobic bacteria, we show that P. micra phylotype A alters the DNA methylation profile promoters of key tumor-suppressor genes, oncogenes, and genes involved in epithelial-mesenchymal transition. In colonic mucosa of CRC patients carrying P. micra phylotype A, we found similar DNA methylation alterations, together with significant enrichment of differentially expressed genes in pathways involved in inflammation, cell adhesion, and regulation of actin cytoskeleton, providing evidence of P. micra's possible role in the carcinogenic process.