Limits...
The PagN protein of Salmonella enterica serovar Typhimurium is an adhesin and invasin.

Lambert MA, Smith SG - BMC Microbiol. (2008)

Bottom Line: S. enterica sv Typhimurium pagN mutants display a reduction in adhesion to and invasion of epithelial cells.Typhimurium.Finally PagN can be added to an ever-growing repertoire of factors that contribute to the pathogenesis of Salmonella.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Clinical Microbiology, Trinity College Dublin, St James's Hospital, Dublin 8, Ireland. malamber79@gmail.com

ABSTRACT

Background: The pagN gene of Salmonella enterica serovar Typhimurium is a PhoP-regulated gene that is up-regulated during growth within macrophages and in vivo in murine models of infection. The PagN protein displays similarity to the Hek and Tia invasins/adhesins of Escherichia coli. Thus far no function has been ascribed to the PagN protein.

Results: Here we show that the outer membrane located PagN protein mediates agglutination of red blood cells and that this can be masked by LPS. When expressed in Escherichia coli the PagN protein supports adhesion to and invasion of mammalian cells in a manner that is dependent on cytoskeletal rearrangements. S. enterica sv Typhimurium pagN mutants display a reduction in adhesion to and invasion of epithelial cells. Finally, we demonstrate that over-expression of PagN in a SPI-1 mutant can partially compensate for the lack of a functional invasasome.

Conclusion: PagN is an outer membrane protein that may contribute to the virulence of S. Typhimurium. This protein is a haemagglutinin and contributes to the adherence to mammalian cells. In addition, PagN can mediate high-level invasion of CHO-K1 cells. Previously,pagN mutants have been shown to be less competitive in vivo and thus this may be due to their lessened ability to interact with mammalian cells. Finally PagN can be added to an ever-growing repertoire of factors that contribute to the pathogenesis of Salmonella.

Show MeSH

Related in: MedlinePlus

Invasion of HT-29 cells by S. Typhimurium SL1344 and a pagN mutant. Invasion levels were calculated for wild-type S. Typhimurium strain SL1344 and pagN mutant derivative ML6. Levels were also calculated for strain ML6 harboring pML10 (PagN+) or the vector control pBR322. Data represents an average of triplicate wells.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC2553418&req=5

Figure 7: Invasion of HT-29 cells by S. Typhimurium SL1344 and a pagN mutant. Invasion levels were calculated for wild-type S. Typhimurium strain SL1344 and pagN mutant derivative ML6. Levels were also calculated for strain ML6 harboring pML10 (PagN+) or the vector control pBR322. Data represents an average of triplicate wells.

Mentions: Furthermore, the pagN mutant strain ML6 in comparison to SL1344 displayed a five-fold reduction in invasion of HT-29 cells (Fig. 7). The overall levels of invasion in all cases were low since the bacteria were cultured in MM 5.8 medium. Cultivation in this medium results in maximal expression of PagN but the expression SPI-1 system is greatly reduced [22]. The decrease in invasion due to the loss of PagN could be complemented to wild-type levels with plasmid pML10. The introduction of pML10 into strain ML6 resulted in a 10-fold increase in adhesion over wild-type levels (see above). However, a corresponding 10-fold increase in invasion levels by pML10/ML6 was not observed. This may be due to saturation of the host cell functions that PagN might use to induce invasion. In summation PagN can contribute to adherence and to low level invasion in the two cell lines tested by S. Typhimurium SL1344.


The PagN protein of Salmonella enterica serovar Typhimurium is an adhesin and invasin.

Lambert MA, Smith SG - BMC Microbiol. (2008)

Invasion of HT-29 cells by S. Typhimurium SL1344 and a pagN mutant. Invasion levels were calculated for wild-type S. Typhimurium strain SL1344 and pagN mutant derivative ML6. Levels were also calculated for strain ML6 harboring pML10 (PagN+) or the vector control pBR322. Data represents an average of triplicate wells.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2553418&req=5

Figure 7: Invasion of HT-29 cells by S. Typhimurium SL1344 and a pagN mutant. Invasion levels were calculated for wild-type S. Typhimurium strain SL1344 and pagN mutant derivative ML6. Levels were also calculated for strain ML6 harboring pML10 (PagN+) or the vector control pBR322. Data represents an average of triplicate wells.
Mentions: Furthermore, the pagN mutant strain ML6 in comparison to SL1344 displayed a five-fold reduction in invasion of HT-29 cells (Fig. 7). The overall levels of invasion in all cases were low since the bacteria were cultured in MM 5.8 medium. Cultivation in this medium results in maximal expression of PagN but the expression SPI-1 system is greatly reduced [22]. The decrease in invasion due to the loss of PagN could be complemented to wild-type levels with plasmid pML10. The introduction of pML10 into strain ML6 resulted in a 10-fold increase in adhesion over wild-type levels (see above). However, a corresponding 10-fold increase in invasion levels by pML10/ML6 was not observed. This may be due to saturation of the host cell functions that PagN might use to induce invasion. In summation PagN can contribute to adherence and to low level invasion in the two cell lines tested by S. Typhimurium SL1344.

Bottom Line: S. enterica sv Typhimurium pagN mutants display a reduction in adhesion to and invasion of epithelial cells.Typhimurium.Finally PagN can be added to an ever-growing repertoire of factors that contribute to the pathogenesis of Salmonella.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Clinical Microbiology, Trinity College Dublin, St James's Hospital, Dublin 8, Ireland. malamber79@gmail.com

ABSTRACT

Background: The pagN gene of Salmonella enterica serovar Typhimurium is a PhoP-regulated gene that is up-regulated during growth within macrophages and in vivo in murine models of infection. The PagN protein displays similarity to the Hek and Tia invasins/adhesins of Escherichia coli. Thus far no function has been ascribed to the PagN protein.

Results: Here we show that the outer membrane located PagN protein mediates agglutination of red blood cells and that this can be masked by LPS. When expressed in Escherichia coli the PagN protein supports adhesion to and invasion of mammalian cells in a manner that is dependent on cytoskeletal rearrangements. S. enterica sv Typhimurium pagN mutants display a reduction in adhesion to and invasion of epithelial cells. Finally, we demonstrate that over-expression of PagN in a SPI-1 mutant can partially compensate for the lack of a functional invasasome.

Conclusion: PagN is an outer membrane protein that may contribute to the virulence of S. Typhimurium. This protein is a haemagglutinin and contributes to the adherence to mammalian cells. In addition, PagN can mediate high-level invasion of CHO-K1 cells. Previously,pagN mutants have been shown to be less competitive in vivo and thus this may be due to their lessened ability to interact with mammalian cells. Finally PagN can be added to an ever-growing repertoire of factors that contribute to the pathogenesis of Salmonella.

Show MeSH
Related in: MedlinePlus