Acquiring high expression of suilysin enable non-epidemic <i>Streptococccus suis</i> to cause streptococcal toxic shock-like syndrome (STSLS) through NLRP3 inflammasome hyperactivation

Xu, Lei; Lin, Lan; Lü, Xi; Peng, Xiao; Liu, Ran; Wu, Meizhou; Jin, Meilin; Zhang, Anding

doi:10.1080/22221751.2021.1908098

Cited by 9 publications

(5 citation statements)

References 46 publications

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“…The overexpression of Sly in ST1 strain (P1/7-Sly) obviously increased in ammasome activation, causing streptococcal toxic shock-like syndrome (STSLS). However, the strain (P1/7-mSly) overexpressing mutant Sly could not cause a cytokine storm and STSLS (Xu et al 2021). Therefore, selecting a target Sly can provide a new idea and a feasible strategy for preventing the S.suis infections.…”

Section: Discussionmentioning

confidence: 99%

CaMKII promotes ROS-dependent apoptosis induced by Suilysin in PK-15 cells

Dai

Zhao

Xiao

et al. 2023

Preprint

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Background Activation of the multifunctional Ca2+/calmodulin-dependent protein kinase II (CaMKII) is a common intermediate of diverse stimuli-induced cell death. Suilysin(Sly) has toxicity on a variety of cells, however, the underlying mechanism of its effect remains unclear, and the mechanism of CaMKII in Sly-induced cell death has not been reported. Methods CaMKII expression in porcine kidney-15 (PK-15) was detected by RT-qPCR analysis and Western blotting. Morphological analysis, and CCK-8 assay were done to verify that CaMKII promotes cytotoxicity induced by Sly. AO/EB staining, and flow cytometry were used to probe into the role of CaMKII and reactive oxygen species (ROS) in Sly-induced apoptosis. The effect of CaMKII on Sly-induced toxicity in mice was evaluated by pathological tissue slices analysis. Results CaMKII was phosphorylated by Sly in PK-15, and inhibition or knockdown of CaMKII resulted in increased resistance to Sly. In PK-15 pretreated with a CaMKII inhibitor (KN93), Sly bound to the cell membrane was reduced, and the Sly-induced ROS, apoptosis were alleviated. Moreover, pretreatment with N-acetyl-L cysteine (NAC), a ROS scavenger, also blocked Sly-induced apoptosis. In summary, our study demonstrated that CaMKII activation and ROS production were involved in Sly-induced apoptosis. In addition, we identified that KN93 attenuated the damage of Sly to the viscera. Conclusion CaMKII participates in Sly-induced ROS-dependent apoptosis and the toxic effects of Sly in mice.

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Section: Discussionmentioning

confidence: 99%

CaMKII promotes ROS-dependent apoptosis induced by Suilysin in PK-15 cells

Dai

Zhao

Xiao

et al. 2023

Preprint

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“…Virulence factors are promising antiinfection targets and avenues for vaccine development against pathogenic bacteria [ 30 ]. Sly is an important virulence factor that can create pores in the target cellular membrane, resulting in high levels of inflammasomes and meningitis caused by S. suis infection [ 31 , 32 ]. Therefore, the antihemolytic strategy is a new selection in target discovery.…”

Section: Discussionmentioning

confidence: 99%

Theaflavin Ameliorates Streptococcus suis-Induced Infection In Vitro and In Vivo

Gao

Tan

Wang

et al. 2023

IJMS

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Streptococcus suis (S. suis) is one of the most important zoonotic pathogens that threaten the lives of pigs and humans. Even worse, the increasingly severe antimicrobial resistance in S. suis is becoming a global issue. Therefore, there is an urgent need to discover novel antibacterial alternatives for the treatment of S. suis infection. In this study, we investigated theaflavin (TF1), a benzoaphenone compound extracted from black tea, as a potential phytochemical compound against S. suis. TF1 at MIC showed significant inhibitory effects on S. suis growth, hemolytic activity, and biofilm formation, and caused damage to S. suis cells in vitro. TF1 had no cytotoxicity and decreased adherent activity of S. suis to the epithelial cell Nptr. Furthermore, TF1 not only improved the survival rate of S. suis-infected mice but also reduced the bacterial load and the production of IL-6 and TNF-α. A hemolysis test revealed the direct interaction between TF1 and Sly, while molecular docking showed TF1 had a good binding activity with the Glu198, Lys190, Asp111, and Ser374 of Sly. Moreover, virulence-related genes were downregulated in the TF1-treated group. Collectively, our findings suggested that TF1 can be used as a potential inhibitor for treating S. suis infection in view of its antibacterial and antihemolytic activity.

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“…In addition to the evaluation of mortality, experimental infections were also performed to evaluate the cytokine response and bacterial burden during S. suis infection [ 25 ]. At the indicated time points, all mice were euthanized by carbon dioxide inhalation, and blood was collected via cardiac puncture.…”

Section: Methodsmentioning

confidence: 99%

Interleukin-17A Contributes to Bacterial Clearance in a Mouse Model of Streptococcal Toxic Shock-Like Syndrome

Lü

Peng

et al. 2021

Pathogens

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Streptococcus suis (S. suis), an emerging zoonotic pathogen, can cause streptococcal toxic shock-like syndrome (STSLS) in humans with high mortality. STSLS is characterized by high bacterial burden, an inflammatory cytokine storm, multi-organ dysfunction, and ultimately acute host death. Although it has been found that a significantly high level of IL-17A was induced in an NLRP3-dependent manner during STSLS development, the role of IL-17A on S. suis STSLS remains to be elucidated. In this study, we found that the epidemic strain SC 19 caused a significantly higher level of IL-17A than the non-epidemic strain P1/7. In addition, higher bacterial burden was observed from SC 19-infected il17a–/– mice than il17a+/+ mice, although acute death, tissue injury and inflammatory cytokines storm were observed in both types of mice. Furthermore, compared with il17a+/+ mice, the level of neutrophils recruitment was lower in il17a–/– mice, and the levels of induced antimicrobial proteins, such as CRAMP, S100A8 and lipocalin-2, were also decreased in il17a–/– mice. In conclusion, this study demonstrated that IL-17A does not contribute to the severe inflammation, although it may play a minor role for bacterial clearance by inducing antimicrobial proteins and promoting neutrophil recruitment during STSLS.

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Acquiring high expression of suilysin enable non-epidemic Streptococccus suis to cause streptococcal toxic shock-like syndrome (STSLS) through NLRP3 inflammasome hyperactivation

Abstract: View related articlesView Crossmark data Citing articles: 1 View citing articles Acquiring high expression of suilysin enable non-epidemic Streptococccus suis to cause streptococcal toxic shock-like syndrome (STSLS) through NLRP3 inflammasome hyperactivation

Cited by 9 publications

References 46 publications

CaMKII promotes ROS-dependent apoptosis induced by Suilysin in PK-15 cells

CaMKII promotes ROS-dependent apoptosis induced by Suilysin in PK-15 cells

Theaflavin Ameliorates Streptococcus suis-Induced Infection In Vitro and In Vivo

Interleukin-17A Contributes to Bacterial Clearance in a Mouse Model of Streptococcal Toxic Shock-Like Syndrome

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