<b>Internal pH crisis, lysine decarboxylase and the acid tolerance response of <i>Salmonella typhimurium</i></b>

Park, Yong-Keun; Bearson, Bradley L.; Bang, Seong Ho; Bang, Iel Soo; Foster, John W.

doi:10.1046/j.1365-2958.1996.5441070.x

Cited by 176 publications

(146 citation statements)

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“…Rather than exerting a global effect, the inhibitory action of cadaverine appears to be speci®c only to S.¯exneri-induced pro-in¯ammatory responses, as the ability of S. typhimurium, EPEC or imposed gradients of fMLP to induce PMN transepithelial migration was insensitive to cadaverine treatment. From the perspective of bacterial pathogen evolution, it is interesting to note that, unlike S.¯exneri, both wild-type S. typhimurium and EPEC strains express LDC activity (Park et al, 1996;unpublished observations). These observations, in concert with control experiments (see Experimental procedures ), also establish that cadaverine has no effect on the assay or the activity of migrating PMNs.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Shigella flexneri-induced transepithelial migration of polymorphonuclear leucocytes by cadaverine

et al. 1999

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SummaryDysentery caused by Shigella species is characterized by in®ltration of polymorphonuclear leucocytes (PMNs) into the colonic mucosa. Shigella spp. evolved into pathogens by the acquisition of virulence genes and by the deletion of`antivirulence' genes detrimental to its pathogenic lifestyle. An example is cadA (encoding lysine decarboxylase), which is uniformly absent in Shigella spp., whereas it is present in nearly all isolates of the closely related non-pathogen Escherichia coli. Here, using monolayers of T84 cells to model the human intestinal epithelium, we determined that the introduction of cadA into S.¯exneri and the expression of lysine decarboxylase attenuated the bacteria's ability to induce PMN in¯ux across model intestinal epithelium. Such inhibition was caused by cadaverine generated from the decarboxylation of lysine. Cadaverine treatment of model intestinal epithelia speci®cally inhibited S.¯exneri induction of PMN transepithelial migration, while having no effect on the ability of Salmonella or enteropathogenic E. coli (EPEC) to induce PMN migration. These observations not only provide insight into mechanisms of S.¯exneri pathogen evolution and pathogenesis, but also suggest a potential for the use of cadaverine in the treatment of dysentery.

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Section: Discussionmentioning

confidence: 99%

Inhibition of Shigella flexneri-induced transepithelial migration of polymorphonuclear leucocytes by cadaverine

et al. 1999

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“…The latter gene is located within PAI II 536 , however, it is absent from other E. coli strains. Lysine decarboxylase can be involved in acid tolerance by consuming protons and neutralizing the acidic byproducts of carbohydrate fermentation (45). Three copies, each composed of the decarboxylase gene and a lysine͞cadaverine antiporter, exist in the E. coli 536 genome, one of which is located within PAI III (ECP327-ECP328).…”

Section: Small Gene Clusters͞single Genes That May Contribute To Urovmentioning

confidence: 99%

How to become a uropathogen: Comparative genomic analysis of extraintestinal pathogenic Escherichia coli strains

Brzuszkiewicz

Brüggemann

Liesegang

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

329

275

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Uropathogenic Escherichia coli (UPEC) strain 536 (O6:K15:H31) is one of the model organisms of extraintestinal pathogenic E. coli (ExPEC). To analyze this strain's genetic basis of urovirulence, we sequenced the entire genome and compared the data with the genome sequence of UPEC strain CFT073 (O6:K2:H1) and to the available genomes of nonpathogenic E. coli strain MG1655 (K-12) and enterohemorrhagic E. coli. The genome of strain 536 is Ϸ292 kb smaller than that of strain CFT073. Genomic differences between both UPEC are mainly restricted to large pathogenicity islands, parts of which are unique to strain 536 or CFT073. Genome comparison underlines that repeated insertions and deletions in certain parts of the genome contribute to genome evolution. Furthermore, 427 and 432 genes are only present in strain 536 or in both UPEC, respectively. The majority of the latter genes is encoded within smaller horizontally acquired DNA regions scattered all over the genome. Several of these genes are involved in increasing the pathogens' fitness and adaptability. Analysis of virulence-associated traits expressed in the two UPEC O6 strains, together with genome comparison, demonstrate the marked genetic and phenotypic variability among UPEC. The ability to accumulate and express a variety of virulence-associated genes distinguishes ExPEC from many commensals and forms the basis for the individual virulence potential of ExPEC. Accordingly, instead of a common virulence mechanism, different ways exist among ExPEC to cause disease.fitness ͉ genome comparison ͉ uropathogenic Escherichia coli

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“…While it may be tempting to speculate that repression of cadA transcription by Fis may represent a step in the expression of virulence in S. typhimurium, it is not known if lysine decarboxylase activity plays any role in S. typhimurium virulence. However, it is known that cadA contributes to acid tolerance in S. typhimurium (Park et al, 1996) and this may point to a role for Fis in adaptation to pH stress.…”

Section: Genes Involved In Metabolism and Transportmentioning

confidence: 99%

A global role for Fis in the transcriptional control of metabolism and type III secretion in Salmonella enterica serovar Typhimurium

et al. 2004

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Fis is a key DNA-binding protein involved in nucleoid organization and modulation of many DNA transactions, including transcription in enteric bacteria. The regulon of genes whose expression is influenced by Fis in Salmonella enterica serovar Typhimurium (S. typhimurium) has been defined by DNA microarray analysis. These data suggest that Fis plays a central role in coordinating the expression of both metabolic and type III secretion factors. The genes that were most strongly up-regulated by Fis were those involved in virulence and located in the pathogenicity islands SPI-1, SPI-2, SPI-3 and SPI-5. Similarly, motility and flagellar genes required Fis for full expression. This was shown to be a direct effect as purified Fis protein bound to the promoter regions of representative flagella and SPI-2 genes. Genes contributing to aspects of metabolism known to assist the bacterium during survival in the mammalian gut were also Fis-regulated, usually negatively. This category included components of metabolic pathways for propanediol utilization, biotin synthesis, vitamin B 12 transport, fatty acids and acetate metabolism, as well as genes for the glyoxylate bypass of the tricarboxylic acid cycle. Genes found to be positively regulated by Fis included those for ethanolamine utilization. The data reported reveal the central role played by Fis in coordinating the expression of both housekeeping and virulence factors required by S. typhimurium during life in the gut lumen or during systemic infection of host cells. INTRODUCTIONSalmonella enterica serovar Typhimurium (S. typhimurium) is the most common and best studied of the S. enterica serovars that infect humans (Finlay & Brumell, 2000). It is able to infect a range of animal species, including chicken, cattle and mice, and intensive study of this organism is providing important insights into key processes involved in bacterial pathogenesis. In the mouse, S. typhimurium is a facultative intracellular pathogen capable of invading epithelial cells and it has the ability to survive and proliferate within macrophages. The bacterium can be manipulated genetically with relative ease and the complete genome sequence is available (McClelland et al., 2001), allowing a combination of genetic analysis, cell biology and animal infection studies. This multidisciplinary approach has provided a picture of the major events involved when S. typhimurium infects the murine host. Following ingestion and passage through the stomach, the bacteria cross the lining of the intestine by invading the intestinal epithelium, predominantly via M cells. The Salmonellae are subsequently phagocytosed by macrophages before entering the blood stream and establishing a systemic infection (Finlay & Brumell, 2000; Galán, 2001;Groisman & Mouslim, 2000;Holden, 2002;Scherer & Miller, 2001).S. typhimurium is dependent upon the products of a large number of genes (up to 200) to cause infection (Finlay & Brumell, 2000). Some of the virulence genes are located on a 90 kb pathogenicity plasmid, of which the spv gen...

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Internal pH crisis, lysine decarboxylase and the acid tolerance response of Salmonella typhimurium

Cited by 176 publications

References 18 publications

Inhibition of Shigella flexneri-induced transepithelial migration of polymorphonuclear leucocytes by cadaverine

Inhibition of Shigella flexneri-induced transepithelial migration of polymorphonuclear leucocytes by cadaverine

How to become a uropathogen: Comparative genomic analysis of extraintestinal pathogenic Escherichia coli strains

A global role for Fis in the transcriptional control of metabolism and type III secretion in Salmonella enterica serovar Typhimurium

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