The role of the ptsI gene on AI-2 internalization and pathogenesis of avian pathogenic Escherichia coli

The LuxS/AI-2 quorum sensing mechanism can regulate the physiological functions of avian pathogenic Escherichia coli (APEC) through internalization of the small molecule autoinducer-2 (AI-2). The ptsl gene encodes enzyme I, which participates in the phosphotransferase system (PTS) that regulates the virulence and AI-2 internalization of bacteria. The aim of the present study was to determine the effect of ptsl on AI-2 internalization and other pathogenesis process in APEC using a ptsl mutant of the APEC strain DE17 (serotype 02), namely DE17 Delta ptsI. The results showed that deletion of the ptsl gene changed the rdar (red dry and rough) morphotype and decreased motility and biofilm formation in APEC (p < 0.05). Furthermore, scanning electron microscopy showed that the biofilm structure of DE17 Delta ptsI became sparse and more extracellular, as compared with the wild-type strain DE17. Moreover, AI-2 assay showed that AI-2 was internalized by DE17 Delta ptsI, while the recombinant PtsI protein had no AI-2 binding activity. Furthermore, deletion of the ptsl gene in APEC significantly increased adherence to DF-1 cells (p < 0.05). The 50% lethal dose of DE17 Delta ptsI was decreased by 17.8-fold and the bacterial loads of DE17,opts/were decreased by 13600-, 68.5-, 131-, and 3600-fold in the blood, liver, spleen, and kidney, respectively, as compared to the DE17. Moreover, histopathological analysis showed that the mutant DE17 Delta ptsI was associated with reduced pathological changes in the heart, liver, spleen, and kidney of ducklings, respectively, as compared to the wild-type strain DE17. The results of this study will benefit further studies on the functions of the ptsl in APEC.