Phagocytosis and killing of Streptococcus suis by porcine neutrophils

Chabot‐Roy, Geneviève; Willson, Philip; Segura, Mariela; Lacouture, Sonia; Gottschalk, Marcelo

doi:10.1016/j.micpath.2006.04.001

Cited by 129 publications

(152 citation statements)

References 61 publications

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“…An early theory suggested that S. suis is taken up by MONOs, allowing the bacteria to survive and travel intracellularly in the circulation (80). Neutrophils may play an important role in the pathogenesis of infection, given that infiltration by neutrophils and mononuclear cells is frequently observed in lesions caused by S. suis (8). Our work shows that the ⌬covR mutant survived more than the wild type in human PMNs and MONOs.…”

Section: Discussionmentioning

confidence: 62%

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: 62%

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

Pan

et al. 2009

J Bacteriol

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“…Compared with the parent strains, the isogenic unencapsulated mutants of S. suis serotype 2 were more susceptible to phagocytosis by both macrophages and neutrophils (Benga et al, 2008;Chabot-Roy et al, 2006;Charland et al, 1998;Smith et al, 1999a). Moreover, capsule loss reduced the virulence of S. suis in both mouse and swine models of infection (Charland et al, 1998;Smith et al, 1999a).…”

Section: Discussionmentioning

confidence: 99%

“…However, more than 50 % of the S. suis isolates from porcine endocarditis were shown to be untypable by agglutination tests (Katsumi et al, 1997), although a high percentage of isolates from meningitis and pneumonia were serotypable (Kataoka et al, 1993). Although the polysaccharide capsule is believed to be essential for the virulence of S. suis (Benga et al, 2008;Chabot-Roy et al, 2006;Charland et al, 1998;Smith et al, 1999a), these observations imply that many endocarditis isolates, especially those of serotypes 2 and 1/2, frequently lose their ability to synthesize capsules.To confirm this speculation, we investigated the capsule production of cps2J-positive isolates from porcine endocarditis and meningitis. Furthermore, the genetic backgrounds of several unencapsulated isolates and the biological significance of unencapsulation were examined.…”

mentioning

confidence: 99%

Loss of capsule among Streptococcus suis isolates from porcine endocarditis and its biological significance

Lakkitjaroen

Takamatsu

Okura

et al. 2011

Journal of Medical Microbiology

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Streptococcus suis, particularly serotype 2, is a pathogen of both pigs and humans associated with a wide range of diseases, including meningitis, septicaemia and endocarditis. Among the genes in the capsular polysaccharide biosynthesis (cps) locus, cps2J exists only in the serotype 2 and 1/2 strains; therefore, cps2J-positive strains are suspected to have capsules of serotype 2 or 1/2. Coagglutination using antiserotype 1 and antiserotype 2 sera and/or transmission electron microscopy analysis of 288 cps2J-positive isolates from pigs showed that 32 (100 %) isolates from meningitis were encapsulated, whereas 86 (34 %) of 256 isolates from endocarditis were unencapsulated, indicating that capsule loss often occurred in the isolates from endocarditis. To investigate the genetic backgrounds, we randomly selected 43 unencapsulated isolates and analysed their cps loci by PCR scanning. Among them, 8 and 10 isolates apparently had deletions and insertions, respectively, in cps loci. In addition, a representative unencapsulated isolate and an unencapsulated strain showed adherence to porcine and human platelets, a major virulence determinant for infective endocarditis, to a significantly greater extent than the encapsulated strains. Although the capsule is considered to be an important virulence factor in S. suis, these results suggest that loss of capsular production is beneficial to S. suis in the course of infective endocarditis. INTRODUCTIONStreptococcus suis is a zoonotic pathogen that causes serious diseases, including meningitis, arthritis, septicaemia and endocarditis, in swine and humans (Gottschalk et al., 2007). S. suis strains are classified into more than 30 serotypes according to the different antigenicity of their capsular polysaccharides (Higgins & Gottschalk, 2006). Among them, serotype 2 has been predominantly isolated from both infected pigs and human patients in many countries (Higgins & Gottschalk, 2006;Wertheim et al., 2009). Production of S. suis capsule is mediated by capsular polysaccharide biosynthesis (cps) genes clustered in a single locus of the genome. Among the genes in the cps loci identified to date (Holden et al., 2009;Smith et al., 1999a Smith et al., , b, c, 2000, cps2J has been found only in strains of serotypes 2 and 1/2 (the serotype reacting with both antiserotypes 1 and 2 sera); therefore, this gene is sometimes used as a molecular marker of the two serotypes (Smith et al., 1999c). However, for determination of the serotypes, it is necessary to verify their phenotypes by serotype-specific antisera. Abbreviations: CcpA, catabolite control protein A; GBS, group B Streptococcus; IS, insertion sequence; TEM, transmission electron microscopy.The GenBank/EMBL/DDBJ accession numbers for the nucleotide sequence data reported in this paper are AB627103, AB627104, AB627105, AB627106, AB627107, AB627108, AB627109, AB627110, AB627111 and AB627112 for the inserted sequences of S. suis NL85, NL155, NL171, NL176, NL179, NL184, NL194, NL198, NL201 and NL255, respectively.Two supplementary tab...

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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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Phagocytosis and killing of Streptococcus suis by porcine neutrophils

Cited by 129 publications

References 61 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

Loss of capsule among Streptococcus suis isolates from porcine endocarditis and its biological significance

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

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