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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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Adhesion efficiency of Salmonella Typhimurium to IPEC-J2 cells after pre-incubation with E. coli.Confluent monolayers of IPEC-J2 cells were pre-incubated with E. coli Nissle 1917 (EcN), E. coli 140815 or E. coli MG1655 using an MOI of 100∶1 E. coli to host cells. After two or six hours, cells were washed and infected with non-invasive Salmonella Typhimurium SL1344 hilA-339::kan or SL1344 pEGFP invG-339::kan using an MOI of 100∶1 Salmonella to host cells. Adhesion levels in percent (%) are expressed as adhesion of Salmonella relative to adhesion without pre-incubation with E. coli (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 Salmonella mono-infection.
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pone-0014712-g006: Adhesion efficiency of Salmonella Typhimurium to IPEC-J2 cells after pre-incubation with E. coli.Confluent monolayers of IPEC-J2 cells were pre-incubated with E. coli Nissle 1917 (EcN), E. coli 140815 or E. coli MG1655 using an MOI of 100∶1 E. coli to host cells. After two or six hours, cells were washed and infected with non-invasive Salmonella Typhimurium SL1344 hilA-339::kan or SL1344 pEGFP invG-339::kan using an MOI of 100∶1 Salmonella to host cells. Adhesion levels in percent (%) are expressed as adhesion of Salmonella relative to adhesion without pre-incubation with E. coli (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 Salmonella mono-infection.

Mentions: We determined whether EcN inhibited Salmonella adhesion, which is also a prerequisite for Salmonella invasion. Salmonella adhesion assays were performed with non-invasive S. Typhimurium SL1344 hilA-339::kan. All three E. coli strains showed no effects on Salmonella adhesion to IPEC-J2 cells in pre-incubation experiments (Figure 6). Even after a six-hour pre-incubation period with E. coli, adhesion of S. Typhimurium SL1344 hilA-339::kan was not affected (Figure 6).


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)

Adhesion efficiency of Salmonella Typhimurium to IPEC-J2 cells after pre-incubation with E. coli.Confluent monolayers of IPEC-J2 cells were pre-incubated with E. coli Nissle 1917 (EcN), E. coli 140815 or E. coli MG1655 using an MOI of 100∶1 E. coli to host cells. After two or six hours, cells were washed and infected with non-invasive Salmonella Typhimurium SL1344 hilA-339::kan or SL1344 pEGFP invG-339::kan using an MOI of 100∶1 Salmonella to host cells. Adhesion levels in percent (%) are expressed as adhesion of Salmonella relative to adhesion without pre-incubation with E. coli (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 Salmonella mono-infection.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3040738&req=5

pone-0014712-g006: Adhesion efficiency of Salmonella Typhimurium to IPEC-J2 cells after pre-incubation with E. coli.Confluent monolayers of IPEC-J2 cells were pre-incubated with E. coli Nissle 1917 (EcN), E. coli 140815 or E. coli MG1655 using an MOI of 100∶1 E. coli to host cells. After two or six hours, cells were washed and infected with non-invasive Salmonella Typhimurium SL1344 hilA-339::kan or SL1344 pEGFP invG-339::kan using an MOI of 100∶1 Salmonella to host cells. Adhesion levels in percent (%) are expressed as adhesion of Salmonella relative to adhesion without pre-incubation with E. coli (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 Salmonella mono-infection.
Mentions: We determined whether EcN inhibited Salmonella adhesion, which is also a prerequisite for Salmonella invasion. Salmonella adhesion assays were performed with non-invasive S. Typhimurium SL1344 hilA-339::kan. All three E. coli strains showed no effects on Salmonella adhesion to IPEC-J2 cells in pre-incubation experiments (Figure 6). Even after a six-hour pre-incubation period with E. coli, adhesion of S. Typhimurium SL1344 hilA-339::kan was not affected (Figure 6).

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