Your browser doesn't support javascript.
loading
Lung exposure to lipopolysaccharide causes atherosclerotic plaque destabilisation.
Jaw, Jen Erh; Tsuruta, Masashi; Oh, Yeni; Schipilow, John; Hirano, Yuki; Ngan, David A; Suda, Koichi; Li, Yuexin; Oh, Jin Young; Moritani, Konosuke; Tam, Sheena; Ford, Nancy; van Eeden, Stephan; Wright, Joanne L; Man, S F Paul; Sin, Don D.
Afiliación
  • Jaw JE; Centre for Heart Lung Innovation, University of British Columbia and St Paul's Hospital, Vancouver, Canada Dept of Medicine, Division of Respirology, University of British Columbia, Vancouver, Canada.
  • Tsuruta M; Centre for Heart Lung Innovation, University of British Columbia and St Paul's Hospital, Vancouver, Canada Dept of Surgery, School of Medicine, Keio University, Tokyo, Japan.
  • Oh Y; Centre for Heart Lung Innovation, University of British Columbia and St Paul's Hospital, Vancouver, Canada.
  • Schipilow J; Centre for High-Throughput Phenogenomics, Oral Biological and Medical Sciences, University of British Columbia, Vancouver, Canada.
  • Hirano Y; Centre for Heart Lung Innovation, University of British Columbia and St Paul's Hospital, Vancouver, Canada Dept of Surgery, School of Medicine, Keio University, Tokyo, Japan.
  • Ngan DA; Centre for Heart Lung Innovation, University of British Columbia and St Paul's Hospital, Vancouver, Canada.
  • Suda K; Centre for Heart Lung Innovation, University of British Columbia and St Paul's Hospital, Vancouver, Canada Division of Upper GI, Dept of Surgery, Fujita Health University, Aichi, Japan.
  • Li Y; Centre for Heart Lung Innovation, University of British Columbia and St Paul's Hospital, Vancouver, Canada.
  • Oh JY; Centre for Heart Lung Innovation, University of British Columbia and St Paul's Hospital, Vancouver, Canada Dept of Internal Medicine, Division of Pulmonology, Dongguk University Ilsan Hospital, Goyang, South Korea.
  • Moritani K; Centre for Heart Lung Innovation, University of British Columbia and St Paul's Hospital, Vancouver, Canada Dept of Surgery, School of Medicine, Keio University, Tokyo, Japan.
  • Tam S; Centre for Heart Lung Innovation, University of British Columbia and St Paul's Hospital, Vancouver, Canada.
  • Ford N; Centre for High-Throughput Phenogenomics, Oral Biological and Medical Sciences, University of British Columbia, Vancouver, Canada.
  • van Eeden S; Centre for Heart Lung Innovation, University of British Columbia and St Paul's Hospital, Vancouver, Canada Dept of Medicine, Division of Respirology, University of British Columbia, Vancouver, Canada.
  • Wright JL; Dept of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, Canada.
  • Man SF; Centre for Heart Lung Innovation, University of British Columbia and St Paul's Hospital, Vancouver, Canada Dept of Medicine, Division of Respirology, University of British Columbia, Vancouver, Canada.
  • Sin DD; Centre for Heart Lung Innovation, University of British Columbia and St Paul's Hospital, Vancouver, Canada Dept of Medicine, Division of Respirology, University of British Columbia, Vancouver, Canada don.sin@hli.ubc.ca.
Eur Respir J ; 48(1): 205-15, 2016 07.
Article en En | MEDLINE | ID: mdl-27009170
Epidemiological studies have implicated lung inflammation as a risk factor for acute cardiovascular events, but the underlying mechanisms linking lung injury with cardiovascular events are largely unknown.Our objective was to develop a novel murine model of acute atheromatous plaque rupture related to lung inflammation and to investigate the role of neutrophils in this process.Lipopolysaccharide (LPS; 3 mg·kg(-1)) or saline (control) was instilled directly into the lungs of male apolipoprotein E-null C57BL/6J mice following 8 weeks of a Western-type diet. 24 h later, atheromas in the right brachiocephalic trunk were assessed for stability ex vivo using high-resolution optical projection tomography and histology. 68% of LPS-exposed mice developed vulnerable plaques, characterised by intraplaque haemorrhage and thrombus, versus 12% of saline-exposed mice (p=0.0004). Plaque instability was detectable as early as 8 h post-intratracheal LPS instillation, but not with intraperitoneal instillation. Depletion of circulating neutrophils attenuated plaque rupture.We have established a novel plaque rupture model related to lung injury induced by intratracheal exposure to LPS. In this model, neutrophils play an important role in both lung inflammation and plaque rupture. This model could be useful for screening therapeutic targets to prevent acute vascular events related to lung inflammation.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Apolipoproteínas E / Citocinas / Placa Aterosclerótica / Neutrófilos Tipo de estudio: Etiology_studies / Prognostic_studies / Risk_factors_studies Límite: Animals / Humans / Male Idioma: En Revista: Eur Respir J Año: 2016 Tipo del documento: Article País de afiliación: Canadá Pais de publicación: Reino Unido

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Apolipoproteínas E / Citocinas / Placa Aterosclerótica / Neutrófilos Tipo de estudio: Etiology_studies / Prognostic_studies / Risk_factors_studies Límite: Animals / Humans / Male Idioma: En Revista: Eur Respir J Año: 2016 Tipo del documento: Article País de afiliación: Canadá Pais de publicación: Reino Unido