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Article

Toxic Shock Syndrome Toxin 1 Induces Immune Response via the Activation of NLRP3 Inflammasome

1
Joint International Research Laboratory of Animal Health and Animal Food Safety, College of Veterinary Medicine, Southwest University, Chongqing 400715, China
2
Chongqing Animal Disease Prevention and Control Center, Chongqing 401120, China
3
Department of Zoonoses, Kitasato University School of Veterinary Medicine, Towada 034-8628, Japan
4
Immunology Research Center, Medical Research Institute, Southwest University, Chongqing 402460, China
*
Authors to whom correspondence should be addressed.
Lianci Peng and Jiali Jiang contributed equally to this work.
Received: 10 December 2020 / Revised: 31 December 2020 / Accepted: 12 January 2021 / Published: 18 January 2021
(This article belongs to the Section Bacterial Toxins)
Staphylococcus aureus is a Gram-positive opportunistic pathogen which causes infections in a variety of vertebrates. Virulence factors are the main pathogenesis of S. aureus as a pathogen, which induce the host’s innate and adaptive immune responses. Toxic shock syndrome toxin 1 (TSST-1) is one of the most important virulence factors of S. aureus. However, the role of nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) in TSST-1-induced innate immune response is still unclear. Here, purified recombinant TSST-1 (rTSST-1) was prepared and used to stimulate mouse peritoneal macrophages. The results showed that under the action of adenosine-triphosphate (ATP), rTSST-1 significantly induced interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) production in mouse macrophages and the production was dose-dependent. In addition, rTSST-1+ATP-stimulated cytokine production in macrophage depends on the activation of toll like receptor 4 (TLR4), but not TLR2 on the cells. Furthermore, the macrophages of NLRP3−/− mice stimulated with rTSST-1+ATP showed significantly low levels of IL-1β production compared to that of wild-type mice. These results demonstrated that TSST-1 can induce the expression of inflammatory cytokines in macrophages via the activation of the TLR4 and NLRP3 signaling pathways. Our study provides new information about the mechanism of the TSST-1-inducing host’s innate immune responses. View Full-Text
Keywords: Staphylococcal toxins; toxic shock syndrome toxin 1; inflammasome; interleukin-1β Staphylococcal toxins; toxic shock syndrome toxin 1; inflammasome; interleukin-1β
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MDPI and ACS Style

Peng, L.; Jiang, J.; Chen, T.; Xu, D.; Hou, F.; Huang, Q.; Peng, Y.; Ye, C.; Hu, D.-L.; Fang, R. Toxic Shock Syndrome Toxin 1 Induces Immune Response via the Activation of NLRP3 Inflammasome. Toxins 2021, 13, 68. https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13010068

AMA Style

Peng L, Jiang J, Chen T, Xu D, Hou F, Huang Q, Peng Y, Ye C, Hu D-L, Fang R. Toxic Shock Syndrome Toxin 1 Induces Immune Response via the Activation of NLRP3 Inflammasome. Toxins. 2021; 13(1):68. https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13010068

Chicago/Turabian Style

Peng, Lianci, Jiali Jiang, Tingting Chen, Dongyi Xu, Fengqing Hou, Qingyuan Huang, Yuanyi Peng, Chao Ye, Dong-Liang Hu, and Rendong Fang. 2021. "Toxic Shock Syndrome Toxin 1 Induces Immune Response via the Activation of NLRP3 Inflammasome" Toxins 13, no. 1: 68. https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13010068

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