The phosphate-induced small RNA EsrL promotes virulence, biofilm formation, and intestinal colonization.

are part of the normal intestinal microbiome, but some enterohemorrhagic (EHEC) and enteropathogenic (EPEC) strains can cause potentially life-threatening gastroenteritis. Virulence factors underlying the ability of EHEC and EPEC to cause disease include those encoded in the locus of the enterocyte effacement (LEE) pathogenicity island. Here, we demonstrated that EsrL, a small RNA present in many strains, promoted pathogenicity, adhesion, and biofilm formation in EHEC and EPEC. PhoB, the response regulator of the two-component system that controls cellular responses to phosphate, directly repressed expression under low-phosphate conditions. A phosphate-rich environment, similar to that of the human intestine, relieved PhoB-mediated repression of . EsrL interacted with and stabilized the () transcript, which encodes a transcription factor for LEE genes, leading to increased bacterial adhesion to cultured cells and colonization of the rabbit colon. EsrL also bound to and stabilized the transcript, which encodes a chaperone that is required for the assembly of type 1 pili, resulting in enhanced cell adhesion in pathogenic and enhanced biofilm formation in pathogenic and nonpathogenic . Our findings demonstrate that EsrL stimulates the expression of virulence genes in both EHEC and EPEC under phosphate-rich conditions, thus promoting the pathogenicity of EHEC and EPEC in the nutrient-rich gut environment.