Abstract
Interactions between bacteria and colon cancer cells influence the transcription of the host cell. Yet is it undetermined whether the bacteria itself or the communication between the host and bacteria is responsible for the genomic changes in the eukaryotic cell. Now, we have investigated the genomic and epigenetic consequences of co-culturing colorectal carcinoma cells with membrane vesicles from pathogenic bacteria Vibrio cholerae and non-pathogenic commensal bacteria Escherichia coli. Our study reveals that membrane vesicles from pathogenic and commensal bacteria have a global impact on the gene expression of colon-carcinoma cells. The changes in gene expression correlate positively with both epigenetic changes and chromatin accessibility of promoters at transcription start sites of genes induced by both types of membrane vesicles. Moreover, we have demonstrated that membrane vesicles obtained only from V. cholerae induced the expression of genes associated with epithelial cell differentiation. Altogether, our study suggests that the observed genomic changes in host cells might be due to specific components of membrane vesicles and do not require communication by direct contact with the bacteria.
Highlights
During growth, both Gram-negative and Gram-positive bacteria release membrane vesicles (MVs) from the bacterial surface
In this study we examined the impact of MVs isolated from V. cholerae and E. coli on HCT8 cells from human ileocecal colorectal adenocarcinoma
We identified a total of 1,434 and 685 genes differentially regulated by E. coli MVs and V. cholerae MVs, respectively (Fig. 1B)
Summary
Both Gram-negative and Gram-positive bacteria release membrane vesicles (MVs) from the bacterial surface. MVs secretion can occur in different environments including aquatic environments, during formation of biofilms and in the infected host[1] They are spherical membranous particles with 20–300 nm diameters, and through their formation may entrap common or specific bacterial components such us periplasmic components, lipopolysaccharides (LPS), peptidoglycan, phospholipids, nucleic acids, proteins, ion metabolites, enzymes, and specific bacterial components[2,3,4]. An epidemiological study suggested that an oral bacterium, Fusobacterium nucleatum, might contribute to epigenetic changes in colon carcinoma tissue[37] It is not well understood how the communication between bacteria and host occurs, or whether any released component from bacteria might be responsible of such genomic effects. We aimed to investigate the genomic and epigenetic consequences of co-culturing HCT8 colorectal carcinoma cells with MVs isolated from pathogenic and non-pathogenic commensal bacterial strains, Vibrio cholerae strain C6706 and Escherichia coli K-12 strain MC1061, respectively
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