Deletion of invH gene in Salmonella enterica serovar Typhimurium limits the secretion of Sip effector proteins

2013 ◽  
Vol 15 (1) ◽  
pp. 66-73 ◽  
Author(s):  
Niladri Bhusan Pati ◽  
Vikalp Vishwakarma ◽  
Sangeeta Jaiswal ◽  
Balamurugan Periaswamy ◽  
Wolf-Dietrich Hardt ◽  
...  
Microbiology ◽  
2007 ◽  
Vol 153 (4) ◽  
pp. 1221-1228 ◽  
Author(s):  
M. N Giacomodonato ◽  
S Uzzau ◽  
D Bacciu ◽  
R Caccuri ◽  
S. H Sarnacki ◽  
...  

2010 ◽  
Vol 6 (12) ◽  
pp. 2448 ◽  
Author(s):  
Garry W. Buchko ◽  
George Niemann ◽  
Erin S. Baker ◽  
Mikhail E. Belov ◽  
Richard D. Smith ◽  
...  

2008 ◽  
Vol 77 (1) ◽  
pp. 60-69 ◽  
Author(s):  
Kim Thien Ly ◽  
James E. Casanova

ABSTRACT The intracellular gram-negative bacterial pathogen Salmonella enterica serovar Typhimurium gains entry into nonphagocytic cells by manipulating the assembly of the host actin cytoskeleton. S. enterica serovar Typhimurium entry requires a functional type III secretion system, a conduit through which bacterial effector proteins are directly translocated into the host cytosol. We and others have previously reported the enhancement of tyrosine kinase activities during Salmonella serovar Typhimurium infection; however, neither specific kinases nor their targets have been well characterized. In this study, we investigated the roles of the cellular Abelson tyrosine kinase (c-Abl) and the related protein Arg in the context of serovar Typhimurium infection. We found that bacterial internalization was inhibited by more than 70% in cells lacking both c-Abl and Arg and that treatment of wild-type cells with a pharmaceutical inhibitor of the c-Abl kinase, STI571 (imatinib), reduced serovar Typhimurium invasion efficiency to a similar extent. Bacterial infection led to enhanced phosphorylation of two previously identified c-Abl substrates, the adaptor protein CT10 regulator of kinase (CrkII) and the Abelson-interacting protein Abi1, a component of the WAVE2 complex. Furthermore, overexpression of the nonphosphorylatable form of CrkII resulted in decreased invasion. Taken together, these findings indicate that c-Abl is activated during S. enterica serovar Typhimurium infection and that its phosphorylation of multiple downstream targets is functionally important in bacterial internalization.


2007 ◽  
Vol 51 (8) ◽  
pp. 2867-2876 ◽  
Author(s):  
Aurel Negrea ◽  
Eva Bjur ◽  
Sofia Eriksson Ygberg ◽  
Mikael Elofsson ◽  
Hans Wolf-Watz ◽  
...  

ABSTRACT A collection of nine salicylidene acylhydrazide compounds were tested for their ability to inhibit the activity of virulence-associated type III secretion systems (T3SSs) in Salmonella enterica serovar Typhimurium. The compounds strongly affected Salmonella pathogenicity island 1 (SPI1) T3SS-mediated invasion of epithelial cells and in vitro secretion of SPI1 invasion-associated effector proteins. The use of a SPI1 effector β-lactamase fusion protein implicated intracellular entrapment of the protein construct upon application of a salicylidene acylhydrazide, whereas the use of chromosomal transcriptional gene fusions revealed a compound-mediated transcriptional silencing of SPI1. Salicylidene acylhydrazides also affected intracellular bacterial replication in murine macrophage-like cells and blocked the transport of an epitope-tagged SPI2 effector protein. Two of the compounds significantly inhibited bacterial motility and expression of extracellular flagellin. We conclude that salicylidene acylhydrazides affect bacterial T3SS activity in S. enterica and hence could be used as lead substances when designing specific inhibitors of bacterial T3SSs in order to pharmaceutically intervene with bacterial virulence.


2004 ◽  
Vol 54 (5) ◽  
pp. 1186-1198 ◽  
Author(s):  
Xiuju Jiang ◽  
Olivia W. Rossanese ◽  
Nat F. Brown ◽  
Sonya Kujat-Choy ◽  
Jorge E. Galán ◽  
...  

2007 ◽  
Vol 189 (13) ◽  
pp. 4587-4596 ◽  
Author(s):  
Inge M. V. Thijs ◽  
Sigrid C. J. De Keersmaecker ◽  
Abeer Fadda ◽  
Kristof Engelen ◽  
Hui Zhao ◽  
...  

ABSTRACT The Salmonella enterica serovar Typhimurium HilA protein is the key regulator for the invasion of epithelial cells. By a combination of genome-wide location and transcript analysis, the HilA-dependent regulon has been delineated. Under invasion-inducing conditions, HilA binds to most of the known target genes and a number of new target genes. The sopB, sopE, and sopA genes, encoding effector proteins secreted by the type III secretion system on Salmonella pathogenicity island 1 (SPI-1), were identified as being both bound by HilA and differentially regulated in an HilA mutant. This suggests a cooperative role for HilA and InvF in the regulation of SPI-1-secreted effectors. Also, siiA, the first gene of SPI-4, is both bound by HilA and differentially regulated in an HilA mutant, thus linking this pathogenicity island to the invasion key regulator. Finally, the interactions of HilA with the SPI-2 secretion system gene ssaH and the flagellar gene flhD imply a repressor function for HilA under invasion-inducing conditions.


2000 ◽  
Vol 68 (6) ◽  
pp. 3158-3163 ◽  
Author(s):  
Renée M. Tsolis ◽  
L. Garry Adams ◽  
Michael J. Hantman ◽  
Christina A. Scherer ◽  
Tyler Kimbrough ◽  
...  

ABSTRACT Salmonella pathogenicity island 1 (SPI-1) encodes virulence determinants, which are important for enteropathogenicity in calves. To determine whether the Salmonella entericaserovar Typhimurium SPI-1 effector proteins SspA and SptP are important for enteropathogenicity, strains lacking these proteins were tested during oral infection of calves. Calves infected with asptP mutant or its isogenic parent developed diarrhea and lethal morbidity. In contrast, calves infected with an sspAmutant developed diarrhea, which resolved within 10 days but did not result in mortality. The sspA mutant was recovered from bovine intestinal tissues at numbers similar to those obtained for its isogenic parent and caused marked intestinal lesions. Thus, the severity of pathological changes caused by serovar Typhimurium strains or their ability to cause diarrhea were not predictive of their ability to cause lethal morbidity in calves. We conclude that factors other than or in addition to bacterial colonization, intestinal lesions, or electrolyte loss contribute to lethal morbidity in calves infected with serovar Typhimurium.


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