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E. coli Nissle 1917 Affects Salmonella adhesion to porcine intestinal epithelial cells.

Schierack P, Kleta S, Tedin K, Babila JT, Oswald S, Oelschlaeger TA, Hiemann R, Paetzold S, Wieler LH - PLoS ONE (2011)

Bottom Line: Another E. coli strain expressing F1C fimbriae was also adherent to IPEC-J2 cells, and was similarly inhibitory against Salmonella invasion like EcN.We propose that EcN affects Salmonella adhesion through secretory components.This mechanism appears to be common to many E. coli strains, with strong adherence being a prerequisite for an effective reduction of SiiE-mediated Salmonella adhesion.

View Article: PubMed Central - PubMed

Affiliation: Institut für Mikrobiologie und Tierseuchen, Freie Universität Berlin, Berlin, Germany. Peter.Schierack@HS-Lausitz.de

ABSTRACT

Background: The probiotic Escherichia coli strain Nissle 1917 (EcN) has been shown to interfere in a human in vitro model with the invasion of several bacterial pathogens into epithelial cells, but the underlying molecular mechanisms are not known.

Methodology/principal findings: In this study, we investigated the inhibitory effects of EcN on Salmonella Typhimurium invasion of porcine intestinal epithelial cells, focusing on EcN effects on the various stages of Salmonella infection including intracellular and extracellular Salmonella growth rates, virulence gene regulation, and adhesion. We show that EcN affects the initial Salmonella invasion steps by modulating Salmonella virulence gene regulation and Salmonella SiiE-mediated adhesion, but not extra- and intracellular Salmonella growth. However, the inhibitory activity of EcN against Salmonella invasion always correlated with EcN adhesion capacities. EcN mutants defective in the expression of F1C fimbriae and flagellae were less adherent and less inhibitory toward Salmonella invasion. Another E. coli strain expressing F1C fimbriae was also adherent to IPEC-J2 cells, and was similarly inhibitory against Salmonella invasion like EcN.

Conclusions: We propose that EcN affects Salmonella adhesion through secretory components. This mechanism appears to be common to many E. coli strains, with strong adherence being a prerequisite for an effective reduction of SiiE-mediated Salmonella adhesion.

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Related in: MedlinePlus

Intracellular growth of Salmonella Typhimurium in IPEC-J2 cells after post-incubation with E. coli Nissle 1917.Confluent monolayers of IPEC-J2 cells were infected with Salmonella Typhimurium for one hour using an MOI of 1∶1 Salmonella to host cells. After one additional hour of incubation in media containing gentamicin, IPEC-J2 cells were incubated with E. coli Nissle 1917 (EcN), E. coli 140815 or E. coli MG1655 for two hours using an MOI of 100∶1 E. coli to host cells, followed by incubation in media with gentamicin. Intracellular Salmonella numbers are presented per well of a 24-well plate. The data are the mean ± S.E.M. of at least three separate experiments in duplicate wells.
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pone-0014712-g007: Intracellular growth of Salmonella Typhimurium in IPEC-J2 cells after post-incubation with E. coli Nissle 1917.Confluent monolayers of IPEC-J2 cells were infected with Salmonella Typhimurium for one hour using an MOI of 1∶1 Salmonella to host cells. After one additional hour of incubation in media containing gentamicin, IPEC-J2 cells were incubated with E. coli Nissle 1917 (EcN), E. coli 140815 or E. coli MG1655 for two hours using an MOI of 100∶1 E. coli to host cells, followed by incubation in media with gentamicin. Intracellular Salmonella numbers are presented per well of a 24-well plate. The data are the mean ± S.E.M. of at least three separate experiments in duplicate wells.

Mentions: To test whether EcN might have been able to affect Salmonella post-invasion, EcN and the two control strains were incubated with Salmonella in post-incubation experiments. Here, IPEC-J2 cells were initially infected with Salmonella for one hour, and extracellular Salmonella were inactivated by incubation with gentamicin for another hour. After removal of gentamicin IPEC-J2 cells with intracellular Salmonella were incubated with E. coli for 2 hours and then incubated for up to 20 hours with medium containing gentamicin to kill extracellular bacteria. Intracellular Salmonella were determined at 2, 5 and 24 hours after the initial Salmonella incubation period. As shown in Figure 7, all three E. coli had no effect on intracellular Salmonella growth at 2, 5 as well as 24 hours after the initial Salmonella incubation.


E. coli Nissle 1917 Affects Salmonella adhesion to porcine intestinal epithelial cells.

Schierack P, Kleta S, Tedin K, Babila JT, Oswald S, Oelschlaeger TA, Hiemann R, Paetzold S, Wieler LH - PLoS ONE (2011)

Intracellular growth of Salmonella Typhimurium in IPEC-J2 cells after post-incubation with E. coli Nissle 1917.Confluent monolayers of IPEC-J2 cells were infected with Salmonella Typhimurium for one hour using an MOI of 1∶1 Salmonella to host cells. After one additional hour of incubation in media containing gentamicin, IPEC-J2 cells were incubated with E. coli Nissle 1917 (EcN), E. coli 140815 or E. coli MG1655 for two hours using an MOI of 100∶1 E. coli to host cells, followed by incubation in media with gentamicin. Intracellular Salmonella numbers are presented per well of a 24-well plate. The data are the mean ± S.E.M. of at least three separate experiments in duplicate wells.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3040738&req=5

pone-0014712-g007: Intracellular growth of Salmonella Typhimurium in IPEC-J2 cells after post-incubation with E. coli Nissle 1917.Confluent monolayers of IPEC-J2 cells were infected with Salmonella Typhimurium for one hour using an MOI of 1∶1 Salmonella to host cells. After one additional hour of incubation in media containing gentamicin, IPEC-J2 cells were incubated with E. coli Nissle 1917 (EcN), E. coli 140815 or E. coli MG1655 for two hours using an MOI of 100∶1 E. coli to host cells, followed by incubation in media with gentamicin. Intracellular Salmonella numbers are presented per well of a 24-well plate. The data are the mean ± S.E.M. of at least three separate experiments in duplicate wells.
Mentions: To test whether EcN might have been able to affect Salmonella post-invasion, EcN and the two control strains were incubated with Salmonella in post-incubation experiments. Here, IPEC-J2 cells were initially infected with Salmonella for one hour, and extracellular Salmonella were inactivated by incubation with gentamicin for another hour. After removal of gentamicin IPEC-J2 cells with intracellular Salmonella were incubated with E. coli for 2 hours and then incubated for up to 20 hours with medium containing gentamicin to kill extracellular bacteria. Intracellular Salmonella were determined at 2, 5 and 24 hours after the initial Salmonella incubation period. As shown in Figure 7, all three E. coli had no effect on intracellular Salmonella growth at 2, 5 as well as 24 hours after the initial Salmonella incubation.

Bottom Line: Another E. coli strain expressing F1C fimbriae was also adherent to IPEC-J2 cells, and was similarly inhibitory against Salmonella invasion like EcN.We propose that EcN affects Salmonella adhesion through secretory components.This mechanism appears to be common to many E. coli strains, with strong adherence being a prerequisite for an effective reduction of SiiE-mediated Salmonella adhesion.

View Article: PubMed Central - PubMed

Affiliation: Institut für Mikrobiologie und Tierseuchen, Freie Universität Berlin, Berlin, Germany. Peter.Schierack@HS-Lausitz.de

ABSTRACT

Background: The probiotic Escherichia coli strain Nissle 1917 (EcN) has been shown to interfere in a human in vitro model with the invasion of several bacterial pathogens into epithelial cells, but the underlying molecular mechanisms are not known.

Methodology/principal findings: In this study, we investigated the inhibitory effects of EcN on Salmonella Typhimurium invasion of porcine intestinal epithelial cells, focusing on EcN effects on the various stages of Salmonella infection including intracellular and extracellular Salmonella growth rates, virulence gene regulation, and adhesion. We show that EcN affects the initial Salmonella invasion steps by modulating Salmonella virulence gene regulation and Salmonella SiiE-mediated adhesion, but not extra- and intracellular Salmonella growth. However, the inhibitory activity of EcN against Salmonella invasion always correlated with EcN adhesion capacities. EcN mutants defective in the expression of F1C fimbriae and flagellae were less adherent and less inhibitory toward Salmonella invasion. Another E. coli strain expressing F1C fimbriae was also adherent to IPEC-J2 cells, and was similarly inhibitory against Salmonella invasion like EcN.

Conclusions: We propose that EcN affects Salmonella adhesion through secretory components. This mechanism appears to be common to many E. coli strains, with strong adherence being a prerequisite for an effective reduction of SiiE-mediated Salmonella adhesion.

Show MeSH
Related in: MedlinePlus