Response regulator important in pathogenesis of Streptococcus suis serotype 2

Greeff, Astrid de; Buys, Herma; Alphen, Loek van; Smith, Hilde E.

doi:10.1016/s0882-4010(02)90526-7

Cited by 32 publications

(24 citation statements)

References 20 publications

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“…Since we were unable to determine a 50% lethal dose for S. suis, it was decided to compare the virulence of the ⌬covR mutant with that of the wild-type strain in a competitive-infection assay in piglets. This kind of cocolonization experiment has been successfully applied to determine the virulence of mutants of Actinobacillus pleuropneumoniae and S. suis in piglets (14,15,21). The data showed that the ⌬covR strain was capable of colonizing the most-examined organs, including heart, liver, kidney, and brain, with higher efficiency than the wild-type strain, which indicates that some components regulated by CovR may play roles in the colonization process.…”

Section: Discussionmentioning

confidence: 99%

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The Orphan Response Regulator CovR: a Globally Negative Modulator of Virulence inStreptococcus suisSerotype 2

Pan

et al. 2009

J Bacteriol

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Streptococcus suis serotype 2 is an emerging zoonotic pathogen responsible for a wide range of life-threatening diseases in pigs and humans. However, the pathogenesis of S. suis serotype 2 infection is not well understood. In this study, we report that an orphan response regulator, CovR, globally regulates gene expression and negatively controls the virulence of S. suis 05ZYH33, a streptococcal toxic shock syndrome (STSS)-causing strain. A covR-defective (⌬covR) mutant of 05ZYH33 displayed dramatic phenotypic changes, such as formation of longer chains, production of thicker capsules, and increased hemolytic activity. Adherence of the ⌬covR mutant to epithelial cells was greatly increased, and its resistance to phagocytosis and killing by neutrophils and monocytes was also significantly enhanced. More importantly, inactivation of covR increased the lethality of S. suis serotype 2 in experimental infection of piglets, and this phenotype was restored by covR complementation. Colonization experiments also showed that the ⌬covR mutant exhibited an increased ability to colonize susceptible tissues of piglets. The pleiotropic phenotype of the ⌬covR mutant is in full agreement with the large number of genes controlled by CovR as revealed by transcription profile analysis: 2 genes are positively regulated, and 193 are repressed, including many that encode known or putative virulence factors. These findings suggested that CovR is a global repressor in virulence regulation of STSS-causing S. suis serotype 2.

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Section: Discussionmentioning

confidence: 99%

“…In S. suis serotype 2, at least 15 TCSs have been identified (11). Among them, only the orphan response regulator RevS (14) and the SalK-SalR (46) system have been reported and shown to positively control S. suis serotype 2 virulence. It is known that bacterial virulence is tightly regulated by both positive and negative feedback mechanisms.…”

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confidence: 99%

The Orphan Response Regulator CovR: a Globally Negative Modulator of Virulence inStreptococcus suisSerotype 2

Pan

et al. 2009

J Bacteriol

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“…No less than 16 pleiotropic regulators have been suggested to be involved in modulation of S. suis virulence, which consist of nine transcription factors (five well-studied ones [ adcR , 149 ccpA , 118 , 119 argR , 40 rgg , 31 a Fur-like repressor PerR 150 ] plus four poorly-known transcription factors such as 00SSU0053, treR , nadR , and scrR 100 ), five TCS systems ( sal K- sal R [renamed as suiK-suiR ], 27 , 151 cia R- cia H, 42 ihk-ihr , 152 virR/virS , 153 and nisK-nisR 154 ), and three orphan regulators (CovR, 30 RevSC21, 155 and RevS 156 , 157 ). …”

Section: Molecular Mechanism For Streptococcus Suis Infectionmentioning

confidence: 99%

Streptococcus suisinfection

et al. 2014

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Streptococcus suis (S. suis) is a family of pathogenic gram-positive bacterial strains that represents a primary health problem in the swine industry worldwide. S. suis is also an emerging zoonotic pathogen that causes severe human infections clinically featuring with varied diseases/syndromes (such as meningitis, septicemia, and arthritis). Over the past few decades, continued efforts have made significant progress toward better understanding this zoonotic infectious entity, contributing in part to the elucidation of the molecular mechanism underlying its high pathogenicity. This review is aimed at presenting an updated overview of this pathogen from the perspective of molecular epidemiology, clinical diagnosis and typing, virulence mechanism, and protective antigens contributing to its zoonosis.

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“…An orphan two-component transcriptional regulator can also control the transcription of virulence genes. Knockout strains harboring deletion in the S. suis ciaRH [24] and in the genes revS and revSC21 encoding orphan regulators show decreased adhesion to Hep-2 cells [25,26]. SalK/SalR is another recently described TCS required for the virulence of S. suis in the porcine model, but its role in the regulation of adhesion is not well known [27,28].…”

Section: Virulence Genes With a Role In Adhesionmentioning

confidence: 99%

Bacterial Adhesion of Streptococcus suis to Host Cells and Its Inhibition by Carbohydrate Ligands

Kouki

Pieters

Nilsson

et al. 2013

Biology

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Streptococcus suis is a Gram-positive bacterium, which causes sepsis and meningitis in pigs and humans. This review examines the role of known S. suis virulence factors in adhesion and S. suis carbohydrate-based adhesion mechanisms, as well as the inhibition of S. suis adhesion by anti-adhesion compounds in in vitro assays. Carbohydrate-binding specificities of S. suis have been identified, and these studies have shown that many strains recognize Galα1-4Gal-containing oligosaccharides present in host glycolipids. In the era of increasing antibiotic resistance, new means to treat infections are needed. Since microbial adhesion to carbohydrates is important to establish disease, compounds blocking adhesion could be an alternative to antibiotics. The use of oligosaccharides as drugs is generally hampered by their relatively low affinity (micromolar) to compete with multivalent binding to host receptors. However, screening of a library of chemically modified Galα1-4Gal derivatives has identified compounds that inhibit S. suis adhesion in nanomolar range. Also, design of multivalent Galα1-4Gal-containing dendrimers has resulted in a significant increase of the inhibitory potency of the disaccharide. The S. suis adhesin binding to Galα1-4Gal-oligosaccharides, Streptococcal adhesin P (SadP), was recently identified. It has a Galα1-4Gal-binding N-terminal domain and a C-terminal LPNTG-motif for cell wall anchoring. The carbohydrate-binding domain has no homology to E. coli P fimbrial adhesin, which suggests that these Gram-positive and Gram-negative bacterial adhesins recognizing the same receptor have evolved by convergent evolution. SadP adhesin may represent a promising target for the design of anti-adhesion ligands for the prevention and treatment of S. suis infections.

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Response regulator important in pathogenesis of Streptococcus suis serotype 2

Cited by 32 publications

References 20 publications

The Orphan Response Regulator CovR: a Globally Negative Modulator of Virulence inStreptococcus suisSerotype 2

The Orphan Response Regulator CovR: a Globally Negative Modulator of Virulence inStreptococcus suisSerotype 2

Streptococcus suisinfection

Bacterial Adhesion of Streptococcus suis to Host Cells and Its Inhibition by Carbohydrate Ligands

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