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Neutrophil extracellular traps induce pyroptosis of pulmonary microvascular endothelial cells by activating the NLRP3 inflammasome.
Zhao, Peipei; Zhu, Jiarui; Bai, Ling; Ma, Wenlan; Li, Feifei; Zhang, Cen; Zhao, Liangtao; Wang, Liuyang; Zhang, Sigong.
Afiliación
  • Zhao P; Department of Rheumatology, Lanzhou University Second Hospital, Lanzhou, Gansu, China.
  • Zhu J; The Second Clinical Medical College, Lanzhou University, Lanzhou, Gansu, China.
  • Bai L; Cui Ying Biomedical Research Center, Lanzhou University Second Hospital, Lanzhou, Gansu, China.
  • Ma W; Department of Rheumatology, Lanzhou University Second Hospital, Lanzhou, Gansu, China.
  • Li F; The Second Clinical Medical College, Lanzhou University, Lanzhou, Gansu, China.
  • Zhang C; Department of Rheumatology, Lanzhou University Second Hospital, Lanzhou, Gansu, China.
  • Zhao L; The Second Clinical Medical College, Lanzhou University, Lanzhou, Gansu, China.
  • Wang L; Department of Rheumatology, Lanzhou University Second Hospital, Lanzhou, Gansu, China.
  • Zhang S; The Second Clinical Medical College, Lanzhou University, Lanzhou, Gansu, China.
Clin Exp Immunol ; 217(1): 89-98, 2024 Jun 20.
Article en En | MEDLINE | ID: mdl-38517050
ABSTRACT
Excessive formation of neutrophil extracellular traps (NETs) may lead to myositis-related interstitial lung disease (ILD). There is evidence that NETs can directly injure vascular endothelial cells and play a pathogenic role in the inflammatory exudation of ILD. However, the specific mechanism is unclear. This study aimed to investigate the specific mechanism underlying NET-induced injury to human pulmonary microvascular endothelial cells (HPMECs). HPMECs were stimulated with NETs (200 ng/ml) in vitro. Cell death was detected by propidium iodide staining. The morphological changes of the cells were observed by transmission electron microscopy (TEM). Pyroptosis markers were detected by western blot, immunofluorescence, and quantitative real-time polymerase chain reaction, and the related inflammatory factor Interleukin-1ß (IL-1ß) was verified by enzyme-linked immunosorbent assay (ELISA). Compared with the control group, HPMECs mortality increased after NET stimulation, and the number of pyroptosis vacuoles in HPMECs was further observed by TEM. The pulmonary microvascular endothelial cells (PMECs) of the experimental autoimmune myositis mouse model also showed a trend of pyroptosis in vivo. Cell experiment further confirmed the significantly high expression of the NLRP3 inflammasome and pyroptosis-related markers, including GSDMD and inflammatory factor IL-1ß. Pretreated with the NLRP3 inhibitor MCC950, the activation of NLRP3 inflammasome and pyroptosis of HPMECs were effectively inhibited. Our study confirmed that NETs promote pulmonary microvascular endothelial pyroptosis by activating the NLRP3 inflammasome, suggesting that NETs-induced pyroptosis of PMECs may be a potential pathogenic mechanism of inflammatory exudation in ILD.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Células Endoteliales / Inflamasomas / Trampas Extracelulares / Piroptosis / Proteína con Dominio Pirina 3 de la Familia NLR / Pulmón Límite: Animals / Humans Idioma: En Revista: Clin Exp Immunol Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido
Texto completo
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XML
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Células Endoteliales / Inflamasomas / Trampas Extracelulares / Piroptosis / Proteína con Dominio Pirina 3 de la Familia NLR / Pulmón Límite: Animals / Humans Idioma: En Revista: Clin Exp Immunol Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido