Porcine Gastric Mucin Triggers Toxin Production of Enteropathogenic .

Enteropathogenic causes foodborne infections due to the production of pore-forming enterotoxins in the intestine. Before that, spores have to be ingested, survive the stomach passage, and germinate. Thus, before reaching epithelial cells, comes in contact with the intestinal mucus layer. In the present study, different aspects of this interaction were analyzed. Total RNA sequencing revealed major transcriptional changes of strain F837/76 upon incubation with porcine gastric mucin (PGM), comprising genes encoding enterotoxins and further putative virulence factors, as well as proteins involved in adhesion to and degradation of mucin. Indeed, PGM was partially degraded by via secreted, EDTA-sensitive proteases. The amount of enterotoxins detectable in culture media supplemented with PGM was also clearly increased. Tests of further strains revealed that enhancement of enterotoxin production upon contact with PGM is broadly distributed among strains. Interestingly, evidence was found that PGM can also strain-specifically trigger germination of spores and that vegetative cells actively move toward mucin. Overall, our data suggest that is well adapted to the host environment due to massive transcriptome changes upon contact with PGM, attributing mucin an important and, thus far, neglected role in pathogenesis.