Streptococcus suis and group B Streptococcus differ in their interactions with murine macrophages

Segura, M

doi:10.1016/s0928-8244(98)00048-0

Cited by 30 publications

(60 citation statements)

References 17 publications

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“…Once in the bloodstream, S. suis resists phagocytosis and killing by neutrophils and monocytes (Chabot-Roy et al, 2006;Charland et al, 1998;Segura et al, 1998;Smith et al, 1999). In the event that S. suis fails to cause acute fatal septicaemia, bacteria are able to reach the CNS via different mechanisms that are only partially elucidated, such as adhesion to, with or without toxicity, and invasion of brain microvascular endothelial cells (BMEC) (Benga et al, 2005;Charland et al, 2000;Vanier et al, 2004) and/or choroid plexus epithelial cells (Tenenbaum et al, 2005(Tenenbaum et al, , 2006.…”

Section: Discussionmentioning

confidence: 99%

Isolation and characterization of α-enolase, a novel fibronectin-binding protein from Streptococcus suis

et al. 2008

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Streptococcus suis is an important swine pathogen that causes meningitis, endocarditis, arthritis and septicaemia. As a zoonotic agent, S. suis also causes similar diseases in humans. Binding of pathogenic bacteria to extracellular matrix components enhances their adhesion to and invasion of host cells. In the present study we isolated and identified a novel fibronectin-binding protein from S. suis. The native protein (designated SsEno) possessed not only high homology with other bacterial enolases but also enolase activity. We cloned, expressed and purified SsEno and showed that it is ubiquitously expressed by all S. suis serotypes and we identified its surface localization using immunoelectron microscopy. ELISA demonstrated that SsEno binds specifically to fibronectin and plasminogen in a lysine-dependent manner. Additional surface plasmon resonance assays demonstrated that SsEno binds to fibronectin or plasminogen with low nanomolar affinity. Inhibition experiments with anti-SsEno antibodies also showed that bacterial SsEno is important for the adhesion to and invasion of brain microvascular endothelial cells by S. suis. Overall, the present work is the first study, to our knowledge, to demonstrate a fibronectinbinding activity of a bacterial enolase, and shows that, similar to other bacterial fibronectin-binding proteins, SsEno may contribute to the virulence of S. suis. INTRODUCTIONStreptococcus suis is a major swine pathogen that causes septicaemia, meningitis, endocarditis and arthritis (Higgins & Gottschalk, 2005). Of the 35 known serotypes, serotype 2 is the most frequently isolated and associated with disease (Higgins & Gottschalk, 2005). It has been proposed that two serotypes (serotypes 32 and 34) be excluded from S. suis and redesignated Streptococcus orisratti (Hill et al., 2005). S. suis, especially serotype 2, has also been described as an important zoonotic agent that affects people in close contact with infected pigs or pork-derived products (Lun et al., 2007). Indeed, an important number of cases of human disease with a high rate of mortality in China were linked directly to a concurrent outbreak of S. suis infection in pigs (Ye et al., 2006).Little is known about S. suis virulence factors. The capsule polysaccharide (CPS) is a critical virulence factor, given that unencapsulated isogenic mutants are completely avirulent and rapidly cleared from the circulation in pig and mouse infection models (Charland et al., 2000;Smith et al., 1999). However, non-virulent strains are also encapsulated, indicating that the virulence of this pathogen is a multifactorial process . Other potential virulence factors have also been described in S. suis, including a haemolysin (suilysin), a 136 kDa muramidase-released protein (MRP), a 110 kDa extracellular factor (EF) protein, a hyaluronidase, a superoxide dismutase, various proteases, a serum opacity factor and different adhesins (Baums et al., 2006;.The pathogenesis of S. suis infection is not fully understood and likely involves many steps . Binding between b...

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Section: Discussionmentioning

confidence: 99%

Isolation and characterization of α-enolase, a novel fibronectin-binding protein from Streptococcus suis

et al. 2008

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“…Our work shows that the ⌬covR mutant survived more than the wild type in human PMNs and MONOs. It is reasonable to explain this phenomenon by the thicker capsule of the ⌬covR strain, since it has been reported that the capsular polysaccharide (CPS) of S. suis protects against phagocytosis and against the bactericidal activity of leukocytes (6,9,48,59,62,63,79). The work of Segura et al demonstrated that S. suis serotype 2 is able to interact with MONOs of human origin, inducing the release of large amounts of the proinflammatory cytokines (61).…”

Section: Discussionmentioning

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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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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“…Like S. suis, GBS possesses a sialic acid-containing capsule and produces a hemolysin, and different virulence potentials are observed among strains (3,25,54). However, although the two species present similar characteristics, the pathogeneses of the infections caused by the two bacteria may be different (38). It is known that GBS can invade BMEC and that GBS hemolysin can injure lung and brain endothelial cells (18,30).…”

Section: Discussionmentioning

confidence: 99%

“…It has been recently demonstrated that the polysaccharide capsule, which is rich in sialic acid (8), confers antiphagocytic properties on S. suis. Acapsular mutants were readily phagocytosed by murine and porcine macrophages, unlike the wildtype strain (7,38,39). Furthermore, S. suis capsule is a virulence factor in the murine and porcine infection models since acapsular mutants were nonpathogenic and more rapidly cleared from the bloodstream than the wild-type strain (7).…”

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confidence: 96%

Streptococcus suis Serotype 2 Interactions with Human Brain Microvascular Endothelial Cells

et al. 2000

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Streptococcus suis serotype 2 is a worldwide causative agent of many forms of swine infection and is also recognized as a zoonotic agent causing human disease, including meningitis. The pathogenesis of S. suis infections is poorly understood. Bacteria circulate in the bloodstream in the nonimmune host until they come in contact with brain microvascular endothelial cells (BMEC) forming the blood-brain barrier. The bacterial polysaccharide capsule confers antiphagocytic properties. It is known that group B streptococci (GBS) invade and damage BMEC, which may be a primary step in the pathogenesis of neonatal meningitis. Interactions between S. suis and human endothelial cells were studied to determine if they differ from those between GBS and endothelial cells. Invasion assays performed with BMEC and human umbilical vein endothelial cells demonstrated that unlike GBS, S. suis serotype 2 could not invade either type of cell. Adherence assays showed that S. suis adhered only to BMEC, whereas GBS adhered to both types of cell. These interactions were not affected by the presence of a capsule, since acapsular mutants from both bacterial species adhered similarly compared to the wild-type strains. Lactate dehydrogenase release measurements indicated that some S. suis strains were highly cytotoxic for BMEC, even more than GBS, whereas others were not toxic at all. Cell damage was related to suilysin (S. suis hemolysin) production, since only suilysin-producing strains were cytotoxic and cytotoxicity could be inhibited by cholesterol and antisuilysin antibodies. It is possible that hemolysin-positive S. suis strains use adherence and suilysin-induced BMEC injury, as opposed to direct cellular invasion, to proceed from the circulation to the central nervous system.

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Streptococcus suis and group B Streptococcus differ in their interactions with murine macrophages

Cited by 30 publications

References 17 publications

Isolation and characterization of α-enolase, a novel fibronectin-binding protein from Streptococcus suis

Isolation and characterization of α-enolase, a novel fibronectin-binding protein from Streptococcus suis

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

Streptococcus suis Serotype 2 Interactions with Human Brain Microvascular Endothelial Cells

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