Staging of the Baboon Response to Group A Streptococci Administered Intramuscularly: A Descriptive Study of the Clinical Symptoms and Clinical Chemical Response Patterns

Taylor, Fletcher B.; Bryant, Amy E.; Blick, Kenneth E.; Hack, Eric; Jansen, Patty M.; Kosanke, Stanley D.; Stevens, Dennis L.

doi:10.1086/520147

Cited by 51 publications

(41 citation statements)

References 43 publications

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“…All of these three factors are regulated by the two-component regulatory system CovRS (33,43,44). Hypervirulent GAS can almost completely inhibit neutrophil infiltration (4,8,(45)(46)(47) and have enhanced expression of the spyCEP and sse genes (33,43,44). Null deletion and mutations of the covS gene cause the severe inhibition of neutrophil infiltration, and SsE is the most critical factor among SsE, ScpA, and SpyCEP for the covS deletion/mutation-mediated enhancement in innate immune evasion and virulence (17).…”

Section: Discussionmentioning

confidence: 99%

Characterization of Streptococcal Platelet-Activating Factor Acetylhydrolase Variants That Are Involved in Innate Immune Evasion

Liu

Xie

et al. 2013

Infect Immun

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Human pathogen group A streptococcus (GAS) has developed mechanisms to subvert innate immunity. We recently reported that the secreted esterase produced by serotype M1 GAS (SsE M1 ) reduces neutrophil recruitment by targeting platelet-activating factor (PAF M28 in a covS deletion mutant of GAS increased neutrophil recruitment and reduced skin infection, whereas in trans expression of SsE M28 in GAS reduced neutrophil infiltration and increased skin invasion in subcutaneous infection of mice. These results suggest that the SsE proteins evolved to target PAF for enhancing innate immune evasion and skin invasion.

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Section: Discussionmentioning

confidence: 99%

Characterization of Streptococcal Platelet-Activating Factor Acetylhydrolase Variants That Are Involved in Innate Immune Evasion

Liu

Xie

et al. 2013

Infect Immun

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“…Yet in the murine model mentioned above, the PT was normal and mice actually demonstrated a hypercoagulable state despite prolongation of the APTT (23). Further, in a nonhuman primate model of M type 3 GAS necrotizing fasciitis and myonecrosis, animals had increased circulating levels of fibrin degradation products and thrombin-antithrombin III complexes, indicating systemic activation of the coagulation system (28). Lastly, the marked DIC observed in the lungs (60%), adrenals (100%), and kidneys (80%) of primates with streptococcal bacteremia (25) and in tissues from humans with StrepTSS (our unpublished data) also suggests that the hemostatic balance is shifted toward a pathological TF-mediated procoagulant state in severe GAS infections (Fig.…”

Section: Vol 71 2003 S Pyogenes Elicits Tissue Factor 1907mentioning

confidence: 95%

M Type 1 and 3 Group A Streptococci Stimulate Tissue Factor-Mediated Procoagulant Activity in Human Monocytes and Endothelial Cells

2003

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Streptococcal toxic shock syndrome (StrepTSS) is an invasive infection characterized by marked coagulopathy, multiple organ failure, and rapid tissue destruction and is strongly associated with M type 1 and 3 group A streptococci (GAS). Initiation of the coagulation cascade with formation of microvascular thrombi contributes to multiple organ failure in human cases of gram-negative bacteremia; however, little is known regarding the mechanism of coagulopathy in StrepTSS. Thus, we investigated the abilities of several strains of M type 1 and 3 GAS isolated from human cases of StrepTSS to stimulate production of tissue factor (TF), the principal initiator of coagulation in vivo. Washed, killed M type 1 and 3 GAS, but not M type 6 GAS, elicited high-level TF-mediated procoagulant activity from both isolated human monocytes and cultured human umbilical vein endothelial cells. M type 1 GAS consistently elicited higher levels of TF from monocytes than did M type 3 GAS. GAS-induced TF synthesis in monocytes did not correlate with production of tumor necrosis factor alpha or interleukin-8. Conversely, M type 3 GAS were consistently more potent than M type 1 GAS in stimulating endothelial cell TF synthesis. These results demonstrate that (i) M type 1 and 3 strains of GAS are potent inducers of TF synthesis, (ii) GAS-induced TF synthesis is not simply an epiphenomenon of cytokine generation, and (iii) induction of TF in endothelial cells and monocytes may be M type specific. In total, these findings suggest that a novel interaction between GAS and host cells contributes to the observed coagulopathy in StrepTSS.

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“…In an experimental baboon model of S. pyogenes myositis, a key difference between fatal and nonfatal infection was the intensity of the inflammatory response. Surviving animals exhibited an intense neutrophilic infiltrate at the site of infection, while nonsurvivors had virtually no influx of neutrophils and extensive bacterial growth in muscle (31). A more tractable model of myositis has recently been developed using zebrafish (26).…”

Section: Gpoamentioning

confidence: 99%

Contribution of Glutathione Peroxidase to the Virulence of Streptococcus pyogenes

et al. 2004

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Glutathione peroxidases are widespread among eukaryotic organisms and function as a major defense against hydrogen peroxide and organic peroxides. However, glutathione peroxidases are not well studied among prokaryotic organisms and have not previously been shown to promote bacterial virulence. Recently, a gene with homology to glutathione peroxidase was shown to contribute to the antioxidant defenses of Streptococcus pyogenes (group A streptococcus). Since this bacterium causes numerous suppurative diseases that require it to thrive in highly inflamed tissue, it was of interest to determine if glutathione peroxidase is important for virulence. In this study, we report that GpoA glutathione peroxidase is the major glutathione peroxidase in S. pyogenes and is essential for S. pyogenes pathogenesis in several murine models that mimic different aspects of streptococcal suppurative disease. In contrast, glutathione peroxidase is not essential for virulence in a zebrafish model of streptococcal myositis, a disease characterized by the absence of an inflammatory cell infiltrate. Taken together, these data suggest that S. pyogenes requires glutathione peroxidase to adapt to oxidative stress that accompanies an inflammatory response, and the data provide the first demonstration of a role for glutathione peroxidase in bacterial virulence. The fact that genes encoding putative glutathione peroxidases are found in the genomes of many pathogenic bacterial species suggests that glutathione peroxidase may have a general role in bacterial pathogenesis.

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Staging of the Baboon Response to Group A Streptococci Administered Intramuscularly: A Descriptive Study of the Clinical Symptoms and Clinical Chemical Response Patterns

Cited by 51 publications

References 43 publications

Characterization of Streptococcal Platelet-Activating Factor Acetylhydrolase Variants That Are Involved in Innate Immune Evasion

Characterization of Streptococcal Platelet-Activating Factor Acetylhydrolase Variants That Are Involved in Innate Immune Evasion

M Type 1 and 3 Group A Streptococci Stimulate Tissue Factor-Mediated Procoagulant Activity in Human Monocytes and Endothelial Cells

Contribution of Glutathione Peroxidase to the Virulence of Streptococcus pyogenes

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