Genetic basis of virulence in Shigella species.

Hale, Thomas L.

doi:10.1128/mmbr.55.2.206-224.1991

Cited by 212 publications

(140 citation statements)

References 119 publications

(231 reference statements)

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“…In some cases, pathogens however take advantage, at least in the initial stages of infection, of the inflammatory response and we expect that the T3S translocation pore may contribute to this phenomenon. Shigella is the most obvious example of this type of pro-inflammatory bacterium endowed with the T3S (Hale, 1991;Perdomo et al, 1994;Sansonetti et al, 2000;Stoycheva and Murdjeva, 2004). Whether T3S translocation pore plays equivalent role in the triggering of pro-inflammatory response by other T3S-encoding bacteria requires further investigation.…”

Section: Discussionmentioning

confidence: 99%

Type III secretion translocation pores of Yersinia enterocolitica trigger maturation and release of pro-inflammatory IL-1β

Shin

Cornelis²

2007

Cellular Microbiology

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Bacteria from the genus Yersinia deliver a number of effectors into host cells via type III secretion (T3S). Injected Yop effectors interfere and prevent pro-inflammatory warning signals by hijacking the host's intracellular machinery. While macrophages infected by wild-type Yersinia enterocolitica did not release mature IL-1beta, macrophages infected by Y. enterocolitica deprived of all effectors released mature IL-1beta. Surprisingly, macrophages infected by Y. enterocolitica deficient for secretion of all T3S proteins, including effectors and translocators, did not release mature IL-1beta. Using different genetic constructs, we show that insertion of T3S translocation pores trigger activation of caspase-1, maturation of proIL-1beta and release of mature IL-1beta, which occurs independently of cell osmotic lysis. These data show that T3S translocation is intrinsically a pro-inflammatory phenomenon. However, in the case of Yersinia, this effect is neutralized by the action of effectors.

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Section: Discussionmentioning

confidence: 99%

Type III secretion translocation pores of Yersinia enterocolitica trigger maturation and release of pro-inflammatory IL-1β

Shin

Cornelis²

2007

Cellular Microbiology

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“…the first consequence of the host-pathogen interaction is the transcriptional activation of the genes that specify the inducible virulence phenotype. Shigella species are enteropathogens that have the capacity to enter epithelial cells of the human colon (Hale, 1991). The genes required for invasion include regulatory genes (Sakai et al, 1988;Adler et al, 1989), the mxi-spa secretion loci (Allaoui et al, 1992(Allaoui et al, , 1993Venkatesan et al, 1992;Sasakawa et al, 1993) and four genes that belong to the same transcription unit: ipgC, ipaB, ipaC and ipaD (Sasakawa et al, 1989;Menard et al, 1993Menard et al, , 1994.…”

Section: Discussionmentioning

confidence: 99%

“…Shigella species are enteropathogens that are able to enter human colonic epithelial cells (reviewed in Hale, 1991). Entry of S.flexneri into epithelial cells is governed by a 31 kb plasmid-bome locus (Maurelli et al, 1985;Sasakawa et al, 1989), which is composed of two divergently transcribed regions.…”

Section: Introductionmentioning

confidence: 99%

The secretion of the Shigella flexneri Ipa invasins is activated by epithelial cells and controlled by IpaB and IpaD.

1994

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Shigella species are enteropathogens that invade epithelial cells of the human colon. Entry into epithelial cells is triggered by the IpaB, IpaC and IpaD proteins which are translocated into the medium through the specific Mxi‐Spa machinery. In vitro, Shigella cells secrete only a small fraction of the Ipa proteins, the majority of which remains in the cytoplasm. We show here that upon interaction with cultured epithelial cells or in the presence of fetal bovine serum, S.flexneri release pre‐synthesized Ipa molecules from the cytoplasm into the environment. Evidence is presented that IpaB and IpaD are essential for both blocking secretion through the Mxi‐Spa translocon in the absence of a secretion‐inducing signal and controlling secretion of the Ipa proteins in the presence of a signal. Subcellular localization and analysis of the molecular interactions of the Ipa proteins indicate that IpaB and IpaD associate transiently in the bacterial envelope. We propose that IpaB and IpaD, by interacting in the secretion apparatus, modulate secretion.

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“…In vitro, cell invasion involves two steps: entry and intercellular dissemination. Genes involved in both steps are carried on a 200 kb virulence plasmid (reviewed by Hale, 1991;Parsot, 1994). A 31 kb fragment of this plasmid is necessary and apparently sufficient for entry into epithelial cells (Maurelli et al, 1985;Sasakawa et al, 1988).…”

Section: Introductionmentioning

confidence: 99%

Induction of type III secretion in Shigella flexneri is associated with differential control of transcription of genes encoding secreted proteins

1998

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Shigella, the etiological agent of human bacillary dysentery, invades the colonic epithelium where it induces an intense inflammatory response. Entry of Shigella into epithelial cells involves a type III secretion machinery, encoded by the mxi and spa operons, and the IpaA-D secreted proteins. In this study, we have identified secreted proteins of 46 and 60 kDa as the products of virA and ipaH9.8, respectively, the latter being a member of the ipaH multigene family. Inactivation of virA did not affect entry into epithelial cells. Using lacZ transcriptional fusions, we found that transcription of virA and four ipaH genes, but not that of the ipaBCDA and mxi operons, was markedly increased during growth in the presence of Congo red and in an ipaD mutant, two conditions in which secretion through the Mxi-Spa machinery is enhanced. Transcription of the virA and ipaH genes was also transiently activated upon entry into epithelial cells. These results suggest that transcription of the virA and ipaH genes is regulated by the type III secretion machinery and that a regulatory cascade differentially controls transcription of genes encoding secreted proteins, some of which, like virA, are not required for entry.

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Genetic basis of virulence in Shigella species.

Cited by 212 publications

References 119 publications

Type III secretion translocation pores of Yersinia enterocolitica trigger maturation and release of pro-inflammatory IL-1β

Type III secretion translocation pores of Yersinia enterocolitica trigger maturation and release of pro-inflammatory IL-1β

The secretion of the Shigella flexneri Ipa invasins is activated by epithelial cells and controlled by IpaB and IpaD.

Induction of type III secretion in Shigella flexneri is associated with differential control of transcription of genes encoding secreted proteins

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