Role of F1C Fimbriae, Flagella, and Secreted Bacterial Components in the Inhibitory Effect of Probiotic Escherichia coli Nissle 1917 on Atypical Enteropathogenic E. coli Infection Original paper

What was studied?

This study investigated how Escherichia coli Nissle 1917 inhibitory mechanisms act against atypical enteropathogenic E. coli by analyzing the contribution of F1C fimbriae, flagella, and secreted bacterial components during early infection steps. The researchers examined how EcN affects aEPEC adhesion, microcolony formation, and type 3 secretion system activity to identify the determinants of EcN’s protective effect. Because the focus keyphrase Escherichia coli Nissle 1917 inhibitory mechanisms appears within this section, the analysis emphasizes adhesion-linked interactions that represent meaningful microbiome signatures relevant to colonization resistance and pathogen exclusion.

Who was studied?

The study used EcN wild-type strains, deletion mutants lacking F1C fimbriae, type 1 fimbriae, or flagella, and control E. coli strains with distinct adhesion profiles. Atypical EPEC strain P2005/03 and typical EPEC strain E2348/69 served as infection models in porcine intestinal epithelial IPEC-J2 cells. This population enabled the authors to compare the colonization behavior of tightly adherent probiotics with that of pathogenic strains while controlling for fimbrial and flagellar expression. Supporting experiments using secreted-protein preparations added mechanistic resolution regarding EcN’s interference with virulence-associated secretion.

Most important findings

The study showed that Escherichia coli Nissle 1917 inhibitory mechanisms rely on a combination of adhesion traits and interference with pathogen virulence. EcN strongly reduced aEPEC adhesion and microcolony formation when present before infection, demonstrating that early colonization steps are critical for inhibition. F1C fimbriae were essential for stable epithelial adhesion, as their deletion removed nearly all adherence and abolished the inhibitory effect. Flagella provided a complementary function by forming a filamentous network that improved surface retention and strengthened competitive positioning. Secreted factors contributed to inhibition during coinfection, with culture supernatants from EcN and control strains reducing aEPEC infection, indicating a non-EcN-specific diffusible inhibitor. EcN supernatants suppressed the secretion of EspA, EspB, and Tir from the EPEC type 3 secretion system, while control strain supernatants produced weaker inhibition.

Key implications

This work suggests that Escherichia coli Nissle 1917 inhibitory mechanisms depend on its strong epithelial adherence and its ability to block early virulence events in atypical EPEC, which provides clinicians with a mechanistic basis for EcN’s efficacy in pathogen-associated diarrhea. The dual action of adhesive structures and secreted components highlights EcN’s capacity to interfere with global features of enteric pathogenesis rather than pathogen-specific traits. These findings reinforce the relevance of adhesion-associated microbiome signatures when identifying or engineering probiotic strains with predictable pathogen exclusion activity. They also indicate that sufficient colonization density is necessary for clinical efficacy, suggesting that dosing strategies that favor early adhesion may enhance therapeutic outcomes in infections involving attaching-effacing pathogens.