Limits...
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.

Show MeSH

Related in: MedlinePlus

Inhibitory effects of focA-positive and focA-negative E. coli isolates on Salmonella Typhimurium invasion.Confluent monolayers of IPEC-J2 cells were pre-incubated with E. coli Nissle 1917 (EcN, focA-positive strain), E. coli WS15C1 (focA-positive strain), E. coli WS30C1 (focA-negative strain) and E. coli WS46C1 (focA-negative strain) using an MOI of 100∶1 E. coli to host cells. After two hours, cells were washed and adhesion efficiencies of E. coli isolates were determined (left side); alternatively, cells were washed after two hours and infected with Salmonella Typhimurium using an MOI of 100∶1 Salmonella to host cells (right side). Adhesion levels in percent (%) were expressed relative to adhesion of EcN. Invasion levels in percent (%) were expressed relative to Salmonella invasion without pre-incubation with bacteria (Salmonella mono-infection). The data are the mean ± S.E.M. of at least three separate experiments in duplicate wells. * = p<0.01 compared to EcN adhesion (left side) or Salmonella mono-infection (right side).
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC3040738&req=5

pone-0014712-g008: Inhibitory effects of focA-positive and focA-negative E. coli isolates on Salmonella Typhimurium invasion.Confluent monolayers of IPEC-J2 cells were pre-incubated with E. coli Nissle 1917 (EcN, focA-positive strain), E. coli WS15C1 (focA-positive strain), E. coli WS30C1 (focA-negative strain) and E. coli WS46C1 (focA-negative strain) using an MOI of 100∶1 E. coli to host cells. After two hours, cells were washed and adhesion efficiencies of E. coli isolates were determined (left side); alternatively, cells were washed after two hours and infected with Salmonella Typhimurium using an MOI of 100∶1 Salmonella to host cells (right side). Adhesion levels in percent (%) were expressed relative to adhesion of EcN. Invasion levels in percent (%) were expressed relative to Salmonella invasion without pre-incubation with bacteria (Salmonella mono-infection). The data are the mean ± S.E.M. of at least three separate experiments in duplicate wells. * = p<0.01 compared to EcN adhesion (left side) or Salmonella mono-infection (right side).

Mentions: To test whether adhesion via F1C fimbriae is essential for a subsequent inhibitory effect of EcN and the specificity of EcN inhibition, we compared adhesion rates as well as inhibition between EcN and another focA gene-positive (WS15C1), and two other focA gene-negative (WS30C1 and WS46C1) E. coli strains. These bacteria all carry the type 1 fimbriae and flagellae and were isolated from the intestine of clinically healthy wild boars [23]. As shown in Figure 8, adhesion rates of the focA gene-positive strain WS15C1 were higher compared to EcN, but focA gene-negative strains WS30C1 and WS46C1 adhered much less compared to EcN. Additionally, these high adhesion rates correlated with high inhibitory effects of EcN and WS15C1 on Salmonella invasion (Figure 8).


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)

Inhibitory effects of focA-positive and focA-negative E. coli isolates on Salmonella Typhimurium invasion.Confluent monolayers of IPEC-J2 cells were pre-incubated with E. coli Nissle 1917 (EcN, focA-positive strain), E. coli WS15C1 (focA-positive strain), E. coli WS30C1 (focA-negative strain) and E. coli WS46C1 (focA-negative strain) using an MOI of 100∶1 E. coli to host cells. After two hours, cells were washed and adhesion efficiencies of E. coli isolates were determined (left side); alternatively, cells were washed after two hours and infected with Salmonella Typhimurium using an MOI of 100∶1 Salmonella to host cells (right side). Adhesion levels in percent (%) were expressed relative to adhesion of EcN. Invasion levels in percent (%) were expressed relative to Salmonella invasion without pre-incubation with bacteria (Salmonella mono-infection). The data are the mean ± S.E.M. of at least three separate experiments in duplicate wells. * = p<0.01 compared to EcN adhesion (left side) or Salmonella mono-infection (right side).
© Copyright Policy
Related In: Results  -  Collection

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

pone-0014712-g008: Inhibitory effects of focA-positive and focA-negative E. coli isolates on Salmonella Typhimurium invasion.Confluent monolayers of IPEC-J2 cells were pre-incubated with E. coli Nissle 1917 (EcN, focA-positive strain), E. coli WS15C1 (focA-positive strain), E. coli WS30C1 (focA-negative strain) and E. coli WS46C1 (focA-negative strain) using an MOI of 100∶1 E. coli to host cells. After two hours, cells were washed and adhesion efficiencies of E. coli isolates were determined (left side); alternatively, cells were washed after two hours and infected with Salmonella Typhimurium using an MOI of 100∶1 Salmonella to host cells (right side). Adhesion levels in percent (%) were expressed relative to adhesion of EcN. Invasion levels in percent (%) were expressed relative to Salmonella invasion without pre-incubation with bacteria (Salmonella mono-infection). The data are the mean ± S.E.M. of at least three separate experiments in duplicate wells. * = p<0.01 compared to EcN adhesion (left side) or Salmonella mono-infection (right side).
Mentions: To test whether adhesion via F1C fimbriae is essential for a subsequent inhibitory effect of EcN and the specificity of EcN inhibition, we compared adhesion rates as well as inhibition between EcN and another focA gene-positive (WS15C1), and two other focA gene-negative (WS30C1 and WS46C1) E. coli strains. These bacteria all carry the type 1 fimbriae and flagellae and were isolated from the intestine of clinically healthy wild boars [23]. As shown in Figure 8, adhesion rates of the focA gene-positive strain WS15C1 were higher compared to EcN, but focA gene-negative strains WS30C1 and WS46C1 adhered much less compared to EcN. Additionally, these high adhesion rates correlated with high inhibitory effects of EcN and WS15C1 on Salmonella invasion (Figure 8).

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