Exposure to Fusobacterium nucleatum induced extensive host cell epigenomic changes and a conserved transcriptomic response dominated by increased inflammation and chemokine gene expression.
F. nucleatum modulates host cell transcriptome and epigenome, driving inflammation and chemokine expression, highlighting its pathogenic mechanisms in cancer.
Fusobacterium nucleatum is a bacterium normally found in the healthy oral cavity but also has an emerging role in colorectal cancer and other cancer settings. The host-microbe interactions of F. nucleatum and its involvement in tumor initiation, progression, and treatment resistance are not fully understood. We explored host cell changes that occur in response to F. nucleatum. We identified key genes differentially expressed in response to various conditions of F. nucleatum exposure and determined that the conserved host cell response to F. nucleatum was dominated by increased inflammation and chemokine gene expression. Additionally, we found extensive host cell epigenomic changes as a novel aspect of host modulation associated with F. nucleatum exposure. These results extend our understanding of F. nucleatum as an emerging pathogen and highlight the importance of considering strain heterogeneity and host cell phenotypic variation when exploring pathogenic mechanisms of F. nucleatum.
Despins et al. (Tue,) conducted a other in Colorectal cancer and other cancer settings. Fusobacterium nucleatum exposure was evaluated on Host cell transcriptome and epigenome changes. Exposure to Fusobacterium nucleatum induced extensive host cell epigenomic changes and a conserved transcriptomic response dominated by increased inflammation and chemokine gene expression.