Enteropathogenic Escherichia coli (EPEC) is a human pathogen that requires initial adhesion to the intestine in order to cause disease. Multiple adhesion factors have been identified in E. coli strains, among them the long polar fimbriae (Lpf), a colonization factor associated with intestinal adhesion. The conditions of Lpf expression are well understood in enterohemorrhagic E. coli (EHEC); however, the expression of EPEC lpf has been found to be repressed under any in vitro condition tested. Therefore, we decided to identify those factors silencing expression of EPEC lpf. Because histone-like nucleoid structuring protein (H-NS) is a known repressor of EHEC lpf, we tested it and found that H-NS is a repressor of EPEC lpf. We also found that the adhesion of the EPEC ⌬hns strain was significantly enhanced compared to the wild-type strain. Because lpf expression was modestly increased in the hns mutant, transposon mutagenesis was performed to find a strain displaying higher lpf expression than EPEC ⌬hns. One Tn5 insertion was identified within the yhjX gene, and further in vitro characterization revealed increased lpf expression and adhesion to Caco-2 cells compared with EPEC ⌬hns. However, in a murine model of intestinal infection, the EPEC ⌬hns and EPEC ⌬hns Tn5 mutants had only a slight change in colonization pattern compared to the wild-type strain. Our data showed that EPEC Lpf is transcribed, but its role in EPEC intestinal colonization requires further analysis.
IMPORTANCEData are presented demonstrating that the long polar fimbriae (lpf) operon in enteropathogenic E. coli (EPEC) is highly regulated; however, derepression occurs by mutagenizing two proteins associated with its control. The study demonstrates that the EPEC lpf operon can be expressed and, therefore, participates in the EPEC adherence phenotype. E scherichia coli bacteria are normally found in the intestines of humans and animals. Most E. coli strains rarely cause disease, except in immunocompromised hosts or in individuals whose normal gastrointestinal barrier is broken (1, 2). However, there are several E. coli strains that carry specific virulence attributes that classify them in specific pathotypes that cause distinct disease in healthy hosts (1). Two of these E. coli pathotypes, enteropathogenic E. coli (EPEC) and enterohemorrhagic E. coli (EHEC), belong to the group of attaching and effacing E. coli (AEEC) strains. AEEC strains are characterized by the presence of a type III secretion system (T3SS) that injects virulence factors into the host cell, mediating the formation of the characterized histopathological attaching and effacing (A/E) lesion (1, 2). EPEC is a leading cause of human infantile diarrhea worldwide (3, 4). EHEC also causes severe human disease, including bloody diarrhea and life-threatening hemolytic uremic syndrome (HUS). Currently, EPEC is estimated to be responsible for 5 to 10% of pediatric diarrhea in developing countries (3). The Global Enteric Multicenter Study (GEMS) showed that some EPEC strains are assoc...