The following is a summary of “Pathogenicity of vancomycin-resistant Enterococcus faecalis to colon cancer cells,” published in the February 2024 issue of Infectious Disease by Zhang et al.
Researchers conducted a retrospective study to examine how vancomycin-resistant Enterococcus faecalis (VREs) affect human colon cells in vitro, assessing their pathogenicity.
They cocultured three E. faecalis isolates (2 VREs and E. faecalis ATCC 29212) with NCM460, HT-29, and HCT116 cells, evaluating changes in cell morphology and bacterial adhesion over time. Interleukin-8 (IL-8) as well as vascular endothelial growth factor A (VEGFA) expression were assessed using RT-qPCR and enzyme-linked immunosorbent assay (ELISA), respectively. Angiogenesis studies utilized cell migration and human umbilical vein endothelial cells (HUVECs) tube formation assays. The activity of the PI3K/AKT/mTOR signaling pathway was examined via Western blotting.
The results showed that the growth and adhesion of E. faecalis at a multiplicity of infection (MOI) of 1:1 were significantly higher than those at an MOI of 100:1 (P<0.05). Compared to E. faecalis ATCC 29212, VREs exhibited reduced invasiveness in NCM460 and HT-29 cells. E. faecalis induced angiogenesis by secreting IL-8 and VEGFA in colon cells, with VRE-infected cells producing significantly higher levels than those infected with the standard strain (P<0.05). Moreover, the PI3K/AKT/mTOR signaling pathway was activated in E. faecalis-infected cells, with VREs displaying greater activation than E. faecalis ATCC 29212 (P<0.05).
Investigators concluded that VREs act as a pro-angiogenic and PI3K/AKT/mTOR activator, fueling CRC development and progression.
Source: bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-024-09133-2
