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TolC, but not AcrB, is involved in the invasiveness of multidrug-resistant Salmonella enterica serovar Typhimurium by increasing type III secretion system-1 expression.
Int J Med Microbiol. 2008 Oct; 298(7-8):561-9.IJ

Abstract

The AcrAB-TolC efflux system is involved in multidrug and bile salt resistances. In addition, this pump has recently been suggested to increase the invasion of Salmonella enterica serovar Typhimurium (S. Typhimurium) into host cells in vitro and could therefore have an important clinical relevance for multidrug-resistant strains. The aim of this study was to investigate the role of the TolC outer membrane channel and the AcrB transporter in the interaction of multidrug-resistant S. Typhimurium strains with eukaryotic cells, especially in relation to the expression of the type III secretion system-1 (TTSS-1) required for Salmonella invasion. Deletion of tolC led to a reduced transcription of the Salmonella pathogenicity island-1 genes sipA, invF and hilA, demonstrating that all genes required for TTSS-1 biosynthesis are down-regulated in this mutant. Consequently, tolC mutants secreted smaller amounts of the TTSS-1 effector proteins SipA and SipC, and invasion tests performed with one mutant showed that it was significantly less able to invade HT-29 epithelial cells than its parental strain. This control seems specific to the TTSS-1 among the three TTSS of Salmonella as no down-regulation of expression of TTSS-2 or flagella was observed in this mutant. By contrast, acrB mutants behaved as their parents except that they secrete a slightly greater amount of SipA and SipC proteins. These data indicate that TolC but not AcrB mediates the uptake of multidrug-resistant S. Typhimurium into target host cells. Therefore, this role of TolC in the invasion of the intestine in addition to its role in bile salt resistance reinforces the interest of targeting TolC for fighting multidrug-resistant Salmonella.

Authors+Show Affiliations

INRA, UR1282 Infectiologie Animale et Santé Publique, IASP, F-37380 Nouzilly, France. Isabelle.Virlogeux@tours.inra.frNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18272427

Citation

Virlogeux-Payant, Isabelle, et al. "TolC, but Not AcrB, Is Involved in the Invasiveness of Multidrug-resistant Salmonella Enterica Serovar Typhimurium By Increasing Type III Secretion System-1 Expression." International Journal of Medical Microbiology : IJMM, vol. 298, no. 7-8, 2008, pp. 561-9.
Virlogeux-Payant I, Baucheron S, Pelet J, et al. TolC, but not AcrB, is involved in the invasiveness of multidrug-resistant Salmonella enterica serovar Typhimurium by increasing type III secretion system-1 expression. Int J Med Microbiol. 2008;298(7-8):561-9.
Virlogeux-Payant, I., Baucheron, S., Pelet, J., Trotereau, J., Bottreau, E., Velge, P., & Cloeckaert, A. (2008). TolC, but not AcrB, is involved in the invasiveness of multidrug-resistant Salmonella enterica serovar Typhimurium by increasing type III secretion system-1 expression. International Journal of Medical Microbiology : IJMM, 298(7-8), 561-9. https://doi.org/10.1016/j.ijmm.2007.12.006
Virlogeux-Payant I, et al. TolC, but Not AcrB, Is Involved in the Invasiveness of Multidrug-resistant Salmonella Enterica Serovar Typhimurium By Increasing Type III Secretion System-1 Expression. Int J Med Microbiol. 2008;298(7-8):561-9. PubMed PMID: 18272427.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - TolC, but not AcrB, is involved in the invasiveness of multidrug-resistant Salmonella enterica serovar Typhimurium by increasing type III secretion system-1 expression. AU - Virlogeux-Payant,Isabelle, AU - Baucheron,Sylvie, AU - Pelet,Julien, AU - Trotereau,Jérôme, AU - Bottreau,Elisabeth, AU - Velge,Philippe, AU - Cloeckaert,Axel, Y1 - 2008/02/12/ PY - 2007/07/05/received PY - 2007/10/26/revised PY - 2007/12/18/accepted PY - 2008/2/15/pubmed PY - 2008/10/25/medline PY - 2008/2/15/entrez SP - 561 EP - 9 JF - International journal of medical microbiology : IJMM JO - Int J Med Microbiol VL - 298 IS - 7-8 N2 - The AcrAB-TolC efflux system is involved in multidrug and bile salt resistances. In addition, this pump has recently been suggested to increase the invasion of Salmonella enterica serovar Typhimurium (S. Typhimurium) into host cells in vitro and could therefore have an important clinical relevance for multidrug-resistant strains. The aim of this study was to investigate the role of the TolC outer membrane channel and the AcrB transporter in the interaction of multidrug-resistant S. Typhimurium strains with eukaryotic cells, especially in relation to the expression of the type III secretion system-1 (TTSS-1) required for Salmonella invasion. Deletion of tolC led to a reduced transcription of the Salmonella pathogenicity island-1 genes sipA, invF and hilA, demonstrating that all genes required for TTSS-1 biosynthesis are down-regulated in this mutant. Consequently, tolC mutants secreted smaller amounts of the TTSS-1 effector proteins SipA and SipC, and invasion tests performed with one mutant showed that it was significantly less able to invade HT-29 epithelial cells than its parental strain. This control seems specific to the TTSS-1 among the three TTSS of Salmonella as no down-regulation of expression of TTSS-2 or flagella was observed in this mutant. By contrast, acrB mutants behaved as their parents except that they secrete a slightly greater amount of SipA and SipC proteins. These data indicate that TolC but not AcrB mediates the uptake of multidrug-resistant S. Typhimurium into target host cells. Therefore, this role of TolC in the invasion of the intestine in addition to its role in bile salt resistance reinforces the interest of targeting TolC for fighting multidrug-resistant Salmonella. SN - 1618-0607 UR - https://www.unboundmedicine.com/medline/citation/18272427/TolC_but_not_AcrB_is_involved_in_the_invasiveness_of_multidrug_resistant_Salmonella_enterica_serovar_Typhimurium_by_increasing_type_III_secretion_system_1_expression_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1438-4221(08)00003-9 DB - PRIME DP - Unbound Medicine ER -