Construction of Urease-Negative Mutants of
            <i>Yersinia enterocolitica</i>
            Serotypes O:3 and O:8: Role of Urease in Virulence and Arthritogenicity

Gripenberg-Lerche, C; Zhang, Lijuan; Ahtonen, Päivi; Toivanen, Paavo; Skurnik, Mikael

doi:10.1128/iai.68.2.942-947.2000

Cited by 45 publications

(30 citation statements)

References 28 publications

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“…In each case, subsequent studies revealed that the in vitro production of each of these virulence factors at a high temperature required specific conditions (36,41). Other virulence factors of Y. enterocolitica are also optimally expressed at low temperatures, including urease and O-antigen outer core (2,9,16,48). A similar scenario has also been described for Vibrio cholerae, which produces much higher levels of cholera toxin in vitro at low temperatures (Ͻ30°C) than at a high temperature (37°C) (40,47).…”

Section: Discussionmentioning

confidence: 99%

YplA Is Exported by the Ysc, Ysa, and Flagellar Type III Secretion Systems ofYersinia enterocolitica

2002

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Yersinia enterocolitica maintains three different pathways for type III protein secretion. Each pathway requires the activity of a specific multicomponent apparatus or type III secretion system (TTSS). Two of the TTSSs are categorized as contact-dependent systems which have been shown in a number of different symbiotic and pathogenic bacteria to influence interactions with host organisms by targeting effector proteins into the cytosol of eukaryotic cells. The third TTSS is required for the assembly of flagella and the secretion of the phospholipase YplA, which has been implicated in Y. enterocolitica virulence. In this study, YplA was expressed from a constitutive promoter in strains that contained only a single TTSS. It was determined that each of the three TTSSs is individually sufficient for YplA secretion. Environmental factors such as temperature, calcium availability, and sodium chloride concentration affected the contribution of each system to extracellular protein secretion and, under some conditions, more than one TTSS appeared to operate simultaneously. This suggests that some proteins might normally be exported by more than one TTSS in Y. enterocolitca.

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Section: Discussionmentioning

confidence: 99%

YplA Is Exported by the Ysc, Ysa, and Flagellar Type III Secretion Systems ofYersinia enterocolitica

2002

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“…Because the natural host infection by Brucella frequently occurs via the oral route, the bacterium has to tolerate low pH during its passage through the digestive tract. Recent work (18) reported that urease-negative mutants of Yersinia enterocolitica were less virulent after intragastric inoculation. Moreover, a previous study of the environmental conditions that B. suis encounters in the host cell has demonstrated that this bacterium survives and remains enclosed in phagosomes which are rapidly acidified.…”

Section: Discussionmentioning

confidence: 99%

Identification of thenikGene Cluster ofBrucella suis: Regulation and Contribution to Urease Activity

et al. 2001

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Analysis of a Brucella suis 1330 gene fused to a gfp reporter, and identified as being induced in J774 murine macrophage-like cells, allowed the isolation of a gene homologous to nikA, the first gene of the Escherichia coli operon encoding the specific transport system for nickel. DNA sequence analysis of the corresponding B. suis nik locus showed that it was highly similar to that of E. coli except for localization of the nikR regulatory gene, which lies upstream from the structural nikABCDE genes and in the opposite orientation. Protein sequence comparisons suggested that the deduced nikABCDE gene products belong to a periplasmic binding proteindependent transport system. The nikA promoter-gfp fusion was activated in vitro by low oxygen tension and metal ion deficiency and was repressed by NiCl 2 excess. Insertional inactivation of nikA strongly reduced the activity of the nickel metalloenzyme urease, which was restored by addition of a nickel excess. Moreover, the nikA mutant of B. suis was functionally complemented with the E. coli nik gene cluster, leading to the recovery of urease activity. Reciprocally, an E. coli strain harboring a deleted nik operon recovered hydrogenase activity by heterologous complementation with the B. suis nik locus. Taking into account these results, we propose that the nik locus of B. suis encodes a nickel transport system. The results further suggest that nickel could enter B. suis via other transport systems. Intracellular growth rates of the B. suis wild-type and nikA mutant strains in human monocytes were similar, indicating that nikA was not essential for this step of infection. We discuss a possible role of nickel transport in maintaining enzymatic activities which could be crucial for survival of the bacteria under the environmental conditions encountered within the host.The gram-negative bacteria Brucella spp. are the etiologic agents of brucellosis, a disease that is encountered worldwide and is endemic in many underdeveloped countries. Six distinct species have been identified in various mammalian hosts, including humans. In cattle, sheep, and goats, the disease still causes important economic losses. Among these species, Brucella melitensis, B. suis, and B. abortus are most frequently associated with pathogenicity in humans, characterized by undulant fever and other, less well-defined clinical symptoms. The infection can be asymptomatic, which may cause diagnostic difficulties and sometimes lead to chronic infections in bones, joints, and the central nervous system. Brucellae belong to the ␣-2 subdivision of the proteobacteria and are therefore phylogenetically related to the plant cell-associated species of the genera Rhizobium and Agrobacterium. Brucella spp. are facultative intracellular parasites that can survive within professional phagocytes. They are able to invade macrophages and to multiply inside acidified phagosomes (36). Among the mechanisms used by brucellae for intracellular survival are the inhibition of phagolysosomal fusion (35) and of tumor necrosis f...

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“…This factor is not essential for systemic infection, but it is necessary for the efficient invasion of the gastrointestinal tract by promoting bacterial uptake by M cells, an event that results in efficient colonization of the Peyer's patches during the earliest phases of infection (31). Urease contributes to virulence by protecting bacteria from the lethal assault of rapid acidification, a situation that Y. enterocolitica endures as it passes though the host gastric regions (16,40).…”

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confidence: 99%

Environmental Regulation and Virulence Attributes of the Ysa Type III Secretion System of Yersinia enterocolitica Biovar 1B

Venecia

Young

2005

Infect Immun

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Pathogenic biovars of Yersinia enterocolitica maintain the well-studied plasmid-encoded Ysc type III secretion (TTS) system, which has a definitive role in virulence. Y. enterocolitica biovar 1B additionally has a distinct chromosomal locus, the Yersinia secretion apparatus pathogenicity island (YSA PI) that encodes the Ysa TTS system. The signals to which the Ysa TTS system responds and its role in virulence remain obscure. This exploratory study was conducted to define environmental cues that promote the expression of Ysa TTS genes and to define how the Ysa TTS system influences bacterium-host interactions. Using a genetic approach, a collection of Y. enterocolitica Ysa TTS mutants was generated by mutagenesis with a transposon carrying promoterless lacZYA. This approach identified genes both within and outside of the YSA PI that contribute to Ysa TTS. Expression of these genes was regulated in response to growth phase, temperature, NaCl, and pH. Additional genetic analysis demonstrated that two regulatory genes encoding components of the YsrR-YsrS (ysrS) and RcsC-YojN-RcsB (rcsB) phosphorelay systems affect the expression of YSA PI genes and each other. The collection of Ysa TTS-defective transposon mutants, along with other strains carrying defined mutations that block Ysa and Ysc TTS, was examined for changes in virulence properties by using the BALB/c mouse model of infection. This analysis revealed that the Ysa TTS system impacts the ability of Y. enterocolitica to colonize gastrointestinal tissues. These results reveal facets of how Y. enterocolitica controls the function of the Ysa TTS system and uncovers a role for the Ysa TTS during the gastrointestinal phase of infection.

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Construction of Urease-Negative Mutants of Yersinia enterocolitica Serotypes O:3 and O:8: Role of Urease in Virulence and Arthritogenicity

Cited by 45 publications

References 28 publications

YplA Is Exported by the Ysc, Ysa, and Flagellar Type III Secretion Systems ofYersinia enterocolitica

YplA Is Exported by the Ysc, Ysa, and Flagellar Type III Secretion Systems ofYersinia enterocolitica

Identification of thenikGene Cluster ofBrucella suis: Regulation and Contribution to Urease Activity

Environmental Regulation and Virulence Attributes of the Ysa Type III Secretion System of Yersinia enterocolitica Biovar 1B

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