Velasco-Carrillo J, Araque-Granadillo M, Ayala-Serrano J, Dávila-Vera D, Peña-Contreras Z, Mendoza-Briceño R

Language: Spanish
References: 20
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ABSTRACT

With the aim of evaluate the pathogenesis in Salmonella Typhimurium strains with mutations in genes invG/invE of Salmonella Pathogenicity Island 1 (SPI-1) and genes ssaJ/ssaK in the SPI-2 models were evaluated ligated intestinal loop associated mouse tissues by observation by transmission electron microscopy (TEM) and the production of mouse systemic salmonellosis. For this, we used six Salmonella strains: S. Typhimurium SL-1344 (control strain) and its derived mutants: ΔinvEG S. Typhimurium SL-1344 (mutant in SPI-1) and ΔssaJK S. Typhimurium SL-1344 (mutant in SPI-2), S. Typhimurium (clinical isolate) and its derived mutants: ΔinvEG S. Typhimurium and ΔssaJK S. Typhimurium. TEM results allowed us to verify the morphological alterations of the intestinal epithelium in mice infected with Salmonella strains whose pathogenicity genes were intact. It was proven invasive power loss only in strains mutated in the SPI-1. Through systemic salmonellosis model mouse we noted the loss of the ability to spread in both mutants. In conclusion, the models allowed us to verify the importance of the invG/invE genes of SPI-1 and ssaJ/ssaK of SPI-2 in the pathogenesis of salmonellosis, using BALB/c mice as an experimental model of infection. These in vivo models are suggested to evaluate mutants of genes involved in the pathogenesis of Salmonella, since they represent an important tool for the understanding of the Salmonella-host interaction.

REFERENCES

1. Morgan E. Salmonella pathogenicity islands. En: Rhen M, Maskell D, Mastroeni P, Threlfall J. Salmonella molecular biology and pathogenesis. London UK: Horizon Bioscience; 2007. p. 67-88.

2. Ramos-Morales F. Impact of Salmonella enteric type III secretion system effectors on the eukaryotic host cell. ISNR Cell Biol 2012; 2012. Disponible en: https://doi.org/10.5402/2012/787934 (Consultado en línea: 13 de febrero de 2016).

3. Romero A, Saraceni P, Merino S, Figueras A, Tomás J, Beatriz Novoa B. The animal model determines the results of Aeromonas virulence factors. Front Microbiol 2016;7(1574). Disponible en: https://doi.org/10.3389/fmicb.2016.01574 (Consultado en línea: 12 de abril de 2017).

4. Swearengen J. Choosing the right animal model for infectious disease research. Animal Model Exp. Med 2018; 1(2):100-108.

5. Valdez Y, Ferreira R, Finlay B. Molecular mechanisms of Salmonella virulence and host resistance. Molecular mechanisms of bacterial infection via the gut. Curr Top Microbiol Immunol 2009;337:93-127.

6. Mastroeni P, Sheppard M. Salmonella infections in the mouse model: host resistance factors and in vivo dynamics of bacterial spread and distribution in the tissues. Microbes Infect 2004;6(4):398-405.

7. Silva G, López HS. Genes involucrados en la patogénesis, persistencia y excreción de Salmonella en modelos animales. Rev Colomb Cienc Pecu 2012;25(1):107-122.

8. Govoni G, Gros P. Macrophage NRAMP1 and its role in resistance to microbial infections. Inflamm Res 1998; 47(7): 277-84.

9. Longa-Briceño A, Peña-Contreras Z, Dávila-Vera D, Mendoza-Briceño R, Palacios-Prü E. Effects of Aeromonas caviae co-cultured in mouse small intestine. Interciencia 2006;31(6):446-50.

10. Ledón T, Rodríguez S, Matos M, Ancheta O, Benchimol M, Reinol F, Fando R. An approach for better visualization of capsular material of Vibrio cholera O139 strains. Acta Microscopica 2012;21(1):1-8.

11. Velasco J, Araque M, Ayala J. Construcción de mutantes de Salmonella enterica por inactivación de los genes invG/invE y ssaJ/ssaK de las islas de patogenicidad 1 y 2. Rev Colomb Biotecnol 2010;12(2):55-66.

12. Jones B, Ghori N, Falkow S. Salmonella typhimurium initiates murine infection by penetrating and destroying the specialized epithelial M cells of the Peyer’s patches. J Exp Med 1994;180:15-23.

13. Wood M, Jones M, Watson P, Hedges S, Wallis T, Galyov E. Identification of a pathogenicity island required for Salmonella enteropathogenicity. Mol Microbiol 1998;29(3):883-91.

14. Netea M, Joosten L, Keuter M, Wagener F, Stalenhoef A, Meer J, et al. Circulating lipoproteins are a crucial component of host defense against invasive Salmonella typhimurium infection. PLoS ONE 2009; 4(1):e4237.https://doi.org/10.1371/journal.pone.0004237

15. Liu T, König R, Sha J, Agar S, Tseng C, Klimpel G, et al. Immunological responses against Salmonella enteric serovar Typhimurium Braun lipoprotein and lipid A mutant strains in Swiss-Webster mice: Potential use as live-attenuated vaccines. Microb Pathog 2008;44(3):224-37.

16. Kaniga K, Bossio J, Galán J. The S. typhimurium invasion genes invF and invG encode homologues of the AraC and PulD family of proteins. Mol Microbiol 1994;13(4):555-568.

17. Clark M, Reed K, Lodge J, Stephen J, Hirst B, Jepson M. Invasion of murine intestinal M cells by Salmonella typhimurium inv mutants severely deficient for invasion of cultured cells. Infect Immun1996;64 (10):4363-4368.

18. Crago A, Koronakis V. Salmonella InvG forms a ring-like multimer that requires the InvH lipoprotein for outer membrane localization. Mol Microbiol 1998;30(1):47-56.

19. Coburn B, Li Y, Owen D, Vallance B, Finlay B. Salmonella enteric serovar Typhimurium pathogenicity island 2 is necessary for complete virulence in a mouse model of infectious enterocolitis. Infect Immun 2005;73(6):3219-27.

20. Galán J, Wolf-Watz H. Protein delivery into eukaryotic cells by type III secretion machines. Nat Rev Microbiol 2006;444(7119):567-73.