In vitro phagocytosis and survival of Streptococcus suis capsular type 2 inside murine macrophages

Brazeau, C.; Gottschalk, Marcelo; Vincelette, S.; Martineau-Doizé, B

doi:10.1099/13500872-142-5-1231

Cited by 33 publications

(31 citation statements)

References 35 publications

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“…The growth rates of strains tested in bacterial culture media were similar and thus not pertinent to the observed differences in bacterial survival. For several streptococcal pathogens, extracellular polysaccharide capsule (GAS, GBS, Streptococcus pneumoniae, and S. suis) (4,17,24,37) and surface-associated proteins (GAS and type 3 pneumococci) (1, 12) deter phagocytosis and prevent opsonization of bacteria by complement. We have noted that disease-associated strains of S. iniae display a high buoyancy (turbid) in broth culture, whereas commensal strains have a low buoyancy, forming a granular precipitate (unpublished data) as described for the type strain (ATCC 29178) (27).…”

Section: Discussionmentioning

confidence: 99%

Streptococcus iniaeVirulence Is Associated with a Distinct Genetic Profile

et al. 2001

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Streptococcus iniae causes meningoencephalitis and death in commercial fish species and has recently been identified as an emerging human pathogen producing fulminant soft tissue infection. As identified by pulsedfield gel electrophoresis (PFGE), strains causing disease in either fish or humans belong to a single clone, whereas isolates from nondiseased fish are genetically diverse. In this study, we used in vivo and in vitro models to examine the pathogenicity of disease-associated isolates. Strains with the clonal (disease-associated) PFGE profile were found to cause significant weight loss and bacteremia in a mouse model of subcutaneous infection. As little as 10 2 CFU of a disease-associated strain was sufficient to establish bacteremia, with higher inocula (10 7 ) resulting in increased mortality. In contrast, non-disease-associated (commensal) strains failed to cause bacteremia and weight loss, even at inocula of 10 8 CFU. In addition, disease-associated strains were more resistant to phagocytic clearance in a human whole blood killing assay compared to commensal strains, which were almost entirely eradicated. Disease-associated strains were also cytotoxic to human endothelial cells as measured by lactate dehydrogenase release from host cells. However, both disease-associated and commensal strains adhered to and invaded cultured human epithelial and endothelial cells equally well. While cellular invasion may still contribute to the pathogenesis of invasive S. iniae disease, resistance to phagocytic clearance and direct cytotoxicity appear to be discriminating virulence attributes of the disease-associated clone.

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Section: Discussionmentioning

confidence: 99%

Streptococcus iniaeVirulence Is Associated with a Distinct Genetic Profile

et al. 2001

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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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“…Host protection against infection caused by S. suis is known to be mediated primarily by opsonophagocytosis/killing (27,(51)(52)(53). Whereas published studies have evidenced the essential contribution of specific humoral immunity to the fight against S. suis (22)(23)(24)(25)(26)(27)54), no study has focused on the precise characteristics of protein-and CPS-specific responses after an infection with live S. suis ) or IgM antiprotein or anti-CPS titers were determined by ELISA on days 7 (n ϭ 9), 14 (n ϭ 7), and 21 (n ϭ 7) in surviving mice.…”

Section: Discussionmentioning

confidence: 99%

Antibody Response Specific to the Capsular Polysaccharide Is Impaired in Streptococcus suis Serotype 2-Infected Animals

et al. 2015

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bStreptococcus suis serotype 2 is an extracellular encapsulated bacterium that causes severe septicemia and meningitis in swine and humans. Albeit crucial in the fight against encapsulated bacteria, the nature of the capsular polysaccharide (CPS)-specific antibody (Ab) response during S. suis type 2 infection is unknown. We compared for the first time the features of CPS-specific versus protein-specific Ab responses during experimental infections with live virulent S. suis type 2 in mice. The primary protein-specific Ab response was dominated by both type 1 and 2 IgG subclasses, whereas IgM titers were more modest. The secondary protein-specific Ab response showed all of the features of a memory response with faster kinetics and boosted the titers of all Ig isotypes. In contrast, the primary CPS-specific Ab response was either inexistent or had titers only slightly higher than those in noninfected animals and was essentially composed of IgM. A poor CPS-specific memory response was observed, with only a moderate boost in IgM titers and no IgG. Both protein-and CPS-specific Ab responses were Toll-like receptor 2 independent. By using S. suis type 2 strains of European or North American origin, the poor CPS-specific Ab response was demonstrated to be independent of the genotypic/phenotypic diversity of the strain within serotype 2. Finally, the CPS-specific Ab response was also impaired and lacked isotype switching in S. suis-infected pigs, the natural host of the bacterium. The better resistance of preinfected animals to reinfection with the same strain of S. suis type 2 might thus more likely be related to the development of a protein rather than CPS Ab response.

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In vitro phagocytosis and survival of Streptococcus suis capsular type 2 inside murine macrophages

Cited by 33 publications

References 35 publications

Streptococcus iniaeVirulence Is Associated with a Distinct Genetic Profile

Streptococcus iniaeVirulence Is Associated with a Distinct Genetic Profile

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

Antibody Response Specific to the Capsular Polysaccharide Is Impaired in Streptococcus suis Serotype 2-Infected Animals

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