Abstract
Enterohemorrhagic Escherichia coli (EHEC) strains are food-borne pathogens that can cause different clinical conditions. Shiga toxin 2a and/or 2c (Stx2)-producing E. coli O157:H7 is the serotype most frequently associated with severe human disease. In this work we analyzed the hypothesis that host cells participate in Stx2 production, cell damage, and inflammation during EHEC infection. With this aim, macrophage-differentiated THP-1 cells and the intestinal epithelial cell line HCT-8 were incubated with E. coli O157:H7. A time course analysis of cellular and bacterial survival, Stx2 production, stx2 transcription, and cytokine secretion were analyzed in both human cell lines. We demonstrated that macrophages are able to internalize and kill EHEC. Simultaneously, Stx2 produced by internalized bacteria played a major role in macrophage death. In contrast, HCT-8 cells were completely resistant to EHEC infection. Besides, macrophages and HCT-8 infected cells produce IL-1β and IL-8 inflammatory cytokines, respectively. At the same time, bacterial stx2-specific transcripts were detected only in macrophages after EHEC infection. The interplay between bacteria and host cells led to Stx production, triggering of inflammatory response and cell damage, all of which could contribute to a severe outcome after EHEC infections.
Highlights
Enterohemorrhagic Escherichia coli (EHEC) strains are food-borne pathogens that can cause different clinical conditions, such as self-limited diarrhea, hemorrhagic colitis, and systemic complications, such as hemolytic-uremic syndrome (HUS) [1,2,3,4]
RNA analysis showed the presence of stx2 mRNA for A and B subunits
We have previously demonstrated that biologically active Shiga toxin 2a and/or 2c (Stx2) is produced in vivo after plasmid carrying the stx2 sequence (pStx2) transfection, driven by its own stx2 promoter [20]
Summary
Enterohemorrhagic Escherichia coli (EHEC) strains are food-borne pathogens that can cause different clinical conditions, such as self-limited diarrhea, hemorrhagic colitis, and systemic complications, such as hemolytic-uremic syndrome (HUS) [1,2,3,4]. One of the EHEC strain most frequently associated with severe human disease is E. coli O157:H7 [5]. EHEC enters the gastrointestinal tract, survives the acidic condition of the stomach, and reaches intestine, where adhesion to epithelial cells is the first step in the pathogenic cascade. It has been revealed the preferential binding to the follicle associated epithelium (FAE) of Peyer’s patches in the initial events of EHEC colonization, which could lead to the rapid contact of E. coli O157:H7 with underlying human macrophages [6]. EHEC O157 from clade 8 carries several virulence factors including
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