Role of the Nucleotide-Binding Domain-Like Receptor Protein 3 Inflammasome in the Endothelial Dysfunction of Early Sepsis

Endothelial dysfunction is responsible for multiple organ failure and the high mortality rate of sepsis. Nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome plays an essential role in the progression of sepsis. However, the role of NLRP3 inflammasome in the endothelial dysfunction...

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Vydáno v:	Inflammation Ročník 43; číslo 4; s. 1561 - 1571
Hlavní autoři:	Luo, Minghao, Meng, Jiayu, Yan, Jianghong, Shang, Feifei, Zhang, Ting, Lv, Dingyi, Li, Chang, Yang, Xiyang, Luo, Suxin
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	New York Springer US 01.08.2020 Springer Nature B.V
Témata:	Aorta Biomedical and Life Sciences Biomedicine Cecum Coronary vessels Endothelial cells Endothelium IL-1β Immunology Inflammasomes Interleukin 1 Interleukin 1 receptor antagonist Interleukin 1 receptors Internal Medicine Lipopolysaccharides Mortality MyD88 protein Nitric oxide Nitric-oxide synthase Original Article Pathology Pharmacology/Toxicology Rheumatology Sepsis Therapeutic applications TLR4 protein Toll-like receptors Umbilical vein Vasodilation NLRP3 eNOS endothelial dysfunction sepsis
ISSN:	0360-3997, 1573-2576, 1573-2576
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Abstract	Endothelial dysfunction is responsible for multiple organ failure and the high mortality rate of sepsis. Nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome plays an essential role in the progression of sepsis. However, the role of NLRP3 inflammasome in the endothelial dysfunction of sepsis has not been fully elucidated. In this study, septic mice were induced by cecal ligation and puncture (CLP) operation, and human umbilical vein endothelial cells ( HUVECs) were treated with lipopolysaccharide (LPS). The 24-h survival rate after CLP was observed. Vasodilation function of the aorta was detected by vascular reactivity experiments. Expression of p-eNOS, eNOS, TLR4, MYD88, p-p65, p65, p-ikbα, ikbα, iNOS, NLRP3, and IL-1β in the aorta and HUVECs were determined by Western blot. Our results suggest that the p-eNOS expression was downregulated, the endothelium-dependent relaxation function was impaired, and TLR4, MYD88, p-p65, p-ikbα, iNOS, NLRP3, and IL-1β expression increased after CLP. The onset of death was 12 h after CLP, and the mortality rate was nearly 50% at 24 h after operation. The decline of p-eNOS, endothelium-dependent vasodilation function, and survival rate significantly improved with NLRP3-specific inhibitor MCC950 intervention or NLRP3 knockout in CLP mice. The decrease of p-eNOS in HUVECs induced by LPS was alleviated when pretreated with MCC950 or interleukin-1 receptor antagonist (IL-1Ra). In summary, our results indicate that activation of the NLRP3 inflammasome contributes to the development of endothelial dysfunction of early sepsis in mice, suggesting its potential role as a therapeutic target for the treatment of sepsis.
AbstractList	AbstractEndothelial dysfunction is responsible for multiple organ failure and the high mortality rate of sepsis. Nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome plays an essential role in the progression of sepsis. However, the role of NLRP3 inflammasome in the endothelial dysfunction of sepsis has not been fully elucidated. In this study, septic mice were induced by cecal ligation and puncture (CLP) operation, and human umbilical vein endothelial cells (HUVECs) were treated with lipopolysaccharide (LPS). The 24-h survival rate after CLP was observed. Vasodilation function of the aorta was detected by vascular reactivity experiments. Expression of p-eNOS, eNOS, TLR4, MYD88, p-p65, p65, p-ikbα, ikbα, iNOS, NLRP3, and IL-1β in the aorta and HUVECs were determined by Western blot. Our results suggest that the p-eNOS expression was downregulated, the endothelium-dependent relaxation function was impaired, and TLR4, MYD88, p-p65, p-ikbα, iNOS, NLRP3, and IL-1β expression increased after CLP. The onset of death was 12 h after CLP, and the mortality rate was nearly 50% at 24 h after operation. The decline of p-eNOS, endothelium-dependent vasodilation function, and survival rate significantly improved with NLRP3-specific inhibitor MCC950 intervention or NLRP3 knockout in CLP mice. The decrease of p-eNOS in HUVECs induced by LPS was alleviated when pretreated with MCC950 or interleukin-1 receptor antagonist (IL-1Ra). In summary, our results indicate that activation of the NLRP3 inflammasome contributes to the development of endothelial dysfunction of early sepsis in mice, suggesting its potential role as a therapeutic target for the treatment of sepsis. Endothelial dysfunction is responsible for multiple organ failure and the high mortality rate of sepsis. Nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome plays an essential role in the progression of sepsis. However, the role of NLRP3 inflammasome in the endothelial dysfunction of sepsis has not been fully elucidated. In this study, septic mice were induced by cecal ligation and puncture (CLP) operation, and human umbilical vein endothelial cells (HUVECs) were treated with lipopolysaccharide (LPS). The 24-h survival rate after CLP was observed. Vasodilation function of the aorta was detected by vascular reactivity experiments. Expression of p-eNOS, eNOS, TLR4, MYD88, p-p65, p65, p-ikbα, ikbα, iNOS, NLRP3, and IL-1β in the aorta and HUVECs were determined by Western blot. Our results suggest that the p-eNOS expression was downregulated, the endothelium-dependent relaxation function was impaired, and TLR4, MYD88, p-p65, p-ikbα, iNOS, NLRP3, and IL-1β expression increased after CLP. The onset of death was 12 h after CLP, and the mortality rate was nearly 50% at 24 h after operation. The decline of p-eNOS, endothelium-dependent vasodilation function, and survival rate significantly improved with NLRP3-specific inhibitor MCC950 intervention or NLRP3 knockout in CLP mice. The decrease of p-eNOS in HUVECs induced by LPS was alleviated when pretreated with MCC950 or interleukin-1 receptor antagonist (IL-1Ra). In summary, our results indicate that activation of the NLRP3 inflammasome contributes to the development of endothelial dysfunction of early sepsis in mice, suggesting its potential role as a therapeutic target for the treatment of sepsis. Endothelial dysfunction is responsible for multiple organ failure and the high mortality rate of sepsis. Nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome plays an essential role in the progression of sepsis. However, the role of NLRP3 inflammasome in the endothelial dysfunction of sepsis has not been fully elucidated. In this study, septic mice were induced by cecal ligation and puncture (CLP) operation, and human umbilical vein endothelial cells ( HUVECs) were treated with lipopolysaccharide (LPS). The 24-h survival rate after CLP was observed. Vasodilation function of the aorta was detected by vascular reactivity experiments. Expression of p-eNOS, eNOS, TLR4, MYD88, p-p65, p65, p-ikbα, ikbα, iNOS, NLRP3, and IL-1β in the aorta and HUVECs were determined by Western blot. Our results suggest that the p-eNOS expression was downregulated, the endothelium-dependent relaxation function was impaired, and TLR4, MYD88, p-p65, p-ikbα, iNOS, NLRP3, and IL-1β expression increased after CLP. The onset of death was 12 h after CLP, and the mortality rate was nearly 50% at 24 h after operation. The decline of p-eNOS, endothelium-dependent vasodilation function, and survival rate significantly improved with NLRP3-specific inhibitor MCC950 intervention or NLRP3 knockout in CLP mice. The decrease of p-eNOS in HUVECs induced by LPS was alleviated when pretreated with MCC950 or interleukin-1 receptor antagonist (IL-1Ra). In summary, our results indicate that activation of the NLRP3 inflammasome contributes to the development of endothelial dysfunction of early sepsis in mice, suggesting its potential role as a therapeutic target for the treatment of sepsis. Endothelial dysfunction is responsible for multiple organ failure and the high mortality rate of sepsis. Nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome plays an essential role in the progression of sepsis. However, the role of NLRP3 inflammasome in the endothelial dysfunction of sepsis has not been fully elucidated. In this study, septic mice were induced by cecal ligation and puncture (CLP) operation, and human umbilical vein endothelial cells (HUVECs) were treated with lipopolysaccharide (LPS). The 24-h survival rate after CLP was observed. Vasodilation function of the aorta was detected by vascular reactivity experiments. Expression of p-eNOS, eNOS, TLR4, MYD88, p-p65, p65, p-ikbα, ikbα, iNOS, NLRP3, and IL-1β in the aorta and HUVECs were determined by Western blot. Our results suggest that the p-eNOS expression was downregulated, the endothelium-dependent relaxation function was impaired, and TLR4, MYD88, p-p65, p-ikbα, iNOS, NLRP3, and IL-1β expression increased after CLP. The onset of death was 12 h after CLP, and the mortality rate was nearly 50% at 24 h after operation. The decline of p-eNOS, endothelium-dependent vasodilation function, and survival rate significantly improved with NLRP3-specific inhibitor MCC950 intervention or NLRP3 knockout in CLP mice. The decrease of p-eNOS in HUVECs induced by LPS was alleviated when pretreated with MCC950 or interleukin-1 receptor antagonist (IL-1Ra). In summary, our results indicate that activation of the NLRP3 inflammasome contributes to the development of endothelial dysfunction of early sepsis in mice, suggesting its potential role as a therapeutic target for the treatment of sepsis.Endothelial dysfunction is responsible for multiple organ failure and the high mortality rate of sepsis. Nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome plays an essential role in the progression of sepsis. However, the role of NLRP3 inflammasome in the endothelial dysfunction of sepsis has not been fully elucidated. In this study, septic mice were induced by cecal ligation and puncture (CLP) operation, and human umbilical vein endothelial cells (HUVECs) were treated with lipopolysaccharide (LPS). The 24-h survival rate after CLP was observed. Vasodilation function of the aorta was detected by vascular reactivity experiments. Expression of p-eNOS, eNOS, TLR4, MYD88, p-p65, p65, p-ikbα, ikbα, iNOS, NLRP3, and IL-1β in the aorta and HUVECs were determined by Western blot. Our results suggest that the p-eNOS expression was downregulated, the endothelium-dependent relaxation function was impaired, and TLR4, MYD88, p-p65, p-ikbα, iNOS, NLRP3, and IL-1β expression increased after CLP. The onset of death was 12 h after CLP, and the mortality rate was nearly 50% at 24 h after operation. The decline of p-eNOS, endothelium-dependent vasodilation function, and survival rate significantly improved with NLRP3-specific inhibitor MCC950 intervention or NLRP3 knockout in CLP mice. The decrease of p-eNOS in HUVECs induced by LPS was alleviated when pretreated with MCC950 or interleukin-1 receptor antagonist (IL-1Ra). In summary, our results indicate that activation of the NLRP3 inflammasome contributes to the development of endothelial dysfunction of early sepsis in mice, suggesting its potential role as a therapeutic target for the treatment of sepsis.
Author	Yang, Xiyang Yan, Jianghong Zhang, Ting Lv, Dingyi Luo, Minghao Meng, Jiayu Shang, Feifei Luo, Suxin Li, Chang
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Snippet	Endothelial dysfunction is responsible for multiple organ failure and the high mortality rate of sepsis. Nucleotide-binding domain-like receptor protein 3... AbstractEndothelial dysfunction is responsible for multiple organ failure and the high mortality rate of sepsis. Nucleotide-binding domain-like receptor...
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SubjectTerms	Aorta Biomedical and Life Sciences Biomedicine Cecum Coronary vessels Endothelial cells Endothelium IL-1β Immunology Inflammasomes Interleukin 1 Interleukin 1 receptor antagonist Interleukin 1 receptors Internal Medicine Lipopolysaccharides Mortality MyD88 protein Nitric oxide Nitric-oxide synthase Original Article Pathology Pharmacology/Toxicology Rheumatology Sepsis Therapeutic applications TLR4 protein Toll-like receptors Umbilical vein Vasodilation
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Title	Role of the Nucleotide-Binding Domain-Like Receptor Protein 3 Inflammasome in the Endothelial Dysfunction of Early Sepsis
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