Identification of a pathogenicity island required for Salmonella survival in host cells.

Ochman, Howard; Soncini, Fernando C.; Solomon, Felix; Groisman, Eduardo A.

doi:10.1073/pnas.93.15.7800

Cited by 602 publications

(631 citation statements)

References 33 publications

(16 reference statements)

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“…We found that six different ssa mutants replicate normally in macrophage-like RAW 264.7 cells. The bacterial strain from which mutants in both studies were derived was the same, but Ochman et al (1996) used a technique involving bacterial opsonization before exposure to host cells. It is also conceivable that SPI2 mutants behave differently in RAW 264.7 and J774 cells, or that the spiA mutation has a different phenotype from that of ssa mutant strains.…”

Section: Discussionmentioning

confidence: 99%

“…Another component of the type III secretion system of SPI2 is encoded by ssaC (referred to as orf11 by Shea et al, 1996 and spiA by Ochman et al, 1996). In SPI1 ᮊ Blackwell Science Ltd, Molecular Microbiology, 24, 155-167 (Devereux et al, 1984).…”

Section: Spi2 Secretion-apparatus Genes 157mentioning

confidence: 99%

“…We have used this scheme to designate genes encoding the structural components of the type III secretion system of SPI2 as ssa (secretion system apparatus) genes. We propose that genes encoding the secreted targets of the type III secretion system should be designated sse (secretion system effector) genes, those encoding the two-component regulatory system (Shea et al, 1996;Ochman et al, 1996) as ssr (secretion system regulator) genes, and those encoding chaperones for the secreted proteins of SPI2 as ssc (secretion system chaperone) genes. These designations classify SPI2 genes according to their general functions and support a unified nomenclature for type III secretion system genes.…”

Section: Introductionmentioning

confidence: 99%

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Functional analysis of ssaJ and the ssaK/U operon, 13 genes encoding components of the type III secretion apparatus of Salmonella Pathogenicity Island 2

Hensel

Shea

Raupach

et al. 1997

Molecular Microbiology

163

186

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SummaryWe have investigated the structure and transcriptional organization of 13 genes of Salmonella Pathogenicity Island 2 (SPI2) that encode components of the second type III secretion apparatus of Salmonella typhimurium. ssaK, L, M, V, N, O, P, Q, R, S, T, U constitute one operon of 10 kb. ssaJ lies upstream of ssaK and is the terminal gene of another operon. The deduced products of ssaJ, ssaK, ssaV, ssaN, ssaO, ssaQ, ssaR, ssaS, ssaT, and ssaU show greatest similarity to the Yersinia spp. genes yscJ, yscL, lcrD, yscN, yscO, yscQ, yscR, yscS, yscT, and yscU, respectively. The products of the ssaL, ssaM and ssaP genes do not have significant similarity to products of other type III secretion systems, and might be important for the specific function of the SPI2 type III secretion system. Bacterial strains carrying different ssa mutations display minor alterations in terms of serum sensitivity when compared with the wild-type strain, but none are defective in replication within macrophage-like RAW 264.7 cells. However, some of the ssa mutant strains invade HEp2 cells less efficiently and are less cytotoxic to RAW 264.7 macrophages than the wild-type strain. We show that the invasion defect is correlated with a lack of SipC in culture supernatants of these mutant strains.SipC is a product of the SPI1 type III secretion system of S. typhimurium, and is important for epithelial cell invasion. Therefore, mutations in SPI2 can affect the SPI1 secretion system, which raises the possibility of an interaction between the two type III secretion systems.

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Section: Discussionmentioning

confidence: 99%

Section: Spi2 Secretion-apparatus Genes 157mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Functional analysis of ssaJ and the ssaK/U operon, 13 genes encoding components of the type III secretion apparatus of Salmonella Pathogenicity Island 2

Hensel

Shea

Raupach

et al. 1997

Molecular Microbiology

163

186

View full text Add to dashboard Cite

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“…It is also possible that factors other than immune attack were at play; however, bacterial cell division per se did not seem to be affected because SPI -2 mutations did not impair growth rates of these strains in LB broth (not shown ). Further, although it has been well established that loss of SPI -2 function impairs Salmonella replication within macrophages, 14,15,17,18,29 we found that sseB À , sseC À , and ssrA À mutants grew intracellularly in both B16F10 and Cloudman S91 melanoma cells at the same rate as the parental YS1646 strain ( not shown ). These experiments employed the gentamycin protection assay 18 ( Materials and methods ), and multiple time points were examined over 24 hours.…”

Section: Discussionmentioning

confidence: 58%

Salmonella pathogenicity island-2 and anticancer activity in mice

et al. 2002

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Salmonella enterica servovar Typhimurium is capable of targeting, colonizing, and eliciting growth suppression of tumors in mice. We examined the effects of mutations on this anticancer phenotype in two Salmonella virulence gene clusters. Salmonella pathogenicity island ( SPI ) -1 genes promote systemic invasion from the intestine, whereas SPI -2 genes support systemic survival within macrophages and other cells. Disabling SPI -1 ( prgH À ) strongly reduced invasion in vitro, but had no effect on tumor growth suppression in vivo. However, disabling SPI -2 ( ssaT À ) ablated tumor growth suppression. In addition to ssaT À , mutations in SPI -2 genes sseA, sseB, sseC, sscA, and ssrA also eliminated antitumor activity, whereas mutations in sseF or sseG yielded partial loss of function. Impaired tumor amplification was seen in three SPI -2 mutants tested after intravenous or intratumoral injection. A SPI -2 À strain was unable to suppress tumor growth in CD18 -deficient mice with defective macrophages and neutrophils, suggesting that loss of tumor growth suppression in wild -type mice by SPI -2 mutants was not solely a function of increased susceptibility to immune attack. Thus, SPI -2 is essential for the Salmonella antitumor effects, perhaps by aiding bacterial amplification within tumors, and is the first identified genetic system for this Salmonella phenotype.

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“…Salmonella enterica possesses two distinct virulence-related T3SSs, T3SS1 and T3SS2, that are encoded by genes located in Salmonella pathogenicity islands 1 and 2 (SPI1 and SPI2), respectively [2]. T3SS1 is necessary for the invasion of non-phagocytic cells [3], whereas T3SS2 is induced after invasion and is essential for survival and replication within macrophages [4,5].…”

Section: Introductionmentioning

confidence: 99%

Global impact of Salmonella type III secretion effector SteA on host cells

Cardenal‐Muñoz

Gutiérrez

Ramos‐Morales

2014

Biochemical and Biophysical Research Communications

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Salmonella enterica is a Gram-negative bacterium that causes gastroenteritis, bacteremia and typhoid fever in several animal species including humans. Its virulence is greatly dependent on two type III secretion systems, encoded in pathogenicity islands 1 and 2. These systems translocate proteins called effectors into eukaryotic host cell. Effectors interfere with host signal transduction pathways to allow the internalization of pathogens and their survival and proliferation inside vacuoles. SteA is one of the few Salmonella effectors that are substrates of both type III secretion systems. Here, we used gene arrays and bioinformatics analysis to study the genetic response of human epithelial cells to SteA. We found that constitutive synthesis of SteA in HeLa cells leads to induction of genes related to extracellular matrix organization and regulation of cell proliferation and serine/threonine kinase signaling pathways. SteA also causes repression of genes related to immune processes and regulation of purine nucleotide synthesis and pathway-restricted SMAD protein phosphorylation. In addition, a cell biology approach revealed that epithelial cells expressing steA show altered cell morphology, and decreased cytotoxicity, cell-cell adhesion and migration.

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Identification of a pathogenicity island required for Salmonella survival in host cells.

Cited by 602 publications

References 33 publications

Functional analysis of ssaJ and the ssaK/U operon, 13 genes encoding components of the type III secretion apparatus of Salmonella Pathogenicity Island 2

Functional analysis of ssaJ and the ssaK/U operon, 13 genes encoding components of the type III secretion apparatus of Salmonella Pathogenicity Island 2

Salmonella pathogenicity island-2 and anticancer activity in mice

Global impact of Salmonella type III secretion effector SteA on host cells

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