Inflammation and Vascular Effects after Repeated Intratracheal Instillations of Carbon Black and Lipopolysaccharide

Autor: Majid Sheykhzade, Ulla Vogel, Ditte Marie Jensen, Ali Kermanizadeh, Steffen Loft, Nicklas Raun Jacobsen, Peter Møller, Daniel Vest Christophersen, Håkan Wallin
Jazyk: angličtina
Rok vydání: 2016
Předmět:
0301 basic medicine
Lipopolysaccharides
Neutrophils
Physiology
lcsh:Medicine
medicine.disease_cause
Pathology and Laboratory Medicine
Biochemistry
Vascular Medicine
Bronchoalveolar Lavage
White Blood Cells
Mice
Animal Cells
Blood plasma
Medicine and Health Sciences
lcsh:Science
Immune Response
Lung
Aorta
Brachiocephalic Trunk
Mice
Knockout

Multidisciplinary
medicine.diagnostic_test
Glutathione Disulfide
Neurochemistry
Hematology
Neurotransmitters
Glutathione
Plaque
Atherosclerotic

Body Fluids
medicine.anatomical_structure
Blood
Female
medicine.symptom
Anatomy
Cellular Types
Bronchoalveolar Lavage Fluid
Research Article
medicine.medical_specialty
Biogenic Amines
Serotonin
Immune Cells
Immunology
Inflammation
Blood Plasma
03 medical and health sciences
Signs and Symptoms
Apolipoproteins E
Diagnostic Medicine
Internal medicine
medicine.artery
medicine
Intubation
Intratracheal

Serotonin receptor antagonist
Animals
Blood Cells
business.industry
030111 toxicology
lcsh:R
Biology and Life Sciences
Cell Biology
Pneumonia
Atherosclerosis
Mice
Inbred C57BL

030104 developmental biology
Bronchoalveolar lavage
Endocrinology
Vasoconstriction
Cardiovascular Anatomy
Lesions
Blood Vessels
lcsh:Q
Particulate Matter
business
Peptides
Oxidative stress
Neuroscience
Zdroj: PLoS ONE
Christophersen, D V, Jacobsen, N R, Jensen, D M, Kermanizadeh, A, Sheykhzade, M, Loft, S, Vogel, U B, Wallin, H & Møller, P 2016, ' Inflammation and Vascular Effects after Repeated Intratracheal Instillations of Carbon Black and Lipopolysaccharide ', P L o S One, vol. 11, no. 8, e0160731 . https://doi.org/10.1371/journal.pone.0160731
PLoS ONE, Vol 11, Iss 8, p e0160731 (2016)
ISSN: 1932-6203
Popis: Inflammation and oxidative stress are considered the main drivers of vasomotor dysfunction and progression of atherosclerosis after inhalation of particulate matter. In addition, new studies have shown that particle exposure can induce the level of bioactive mediators in serum, driving vascular-and systemic toxicity. We aimed to investigate if pulmonary inflammation would accelerate nanoparticle-induced atherosclerotic plaque progression in Apolipoprotein E knockout (ApoE-/-) mice. ApoE-/- mice were exposed to vehicle, 8.53 or 25.6 mu g nanosized carbon black (CB) alone or spiked with LPS (0.2 mu g/mouse/exposure; once a week for 10 weeks). Inflammation was determined by counting cells in bronchoalveolar lavage fluid. Serum Amyloid A3 (Saa3) expression and glutathione status were determined in lung tissue. Plaque progression was assessed in the aorta and the brachiocephalic artery. The effect of vasoactive mediators in plasma of exposed ApoE-/- mice was assessed in aorta rings isolated from naive C57BL/6 mice. Pulmonary exposure to CB and/or LPS resulted in pulmonary inflammation with a robust influx of neutrophils. The CB exposure did not promote plaque progression in aorta or BCA. Incubation with 0.5% plasma extracted from CB-exposed ApoE-/- mice caused vasoconstriction in aorta rings isolated from naive mice; this effect was abolished by the treatment with the serotonin receptor antagonist Ketanserin. In conclusion, repeated pulmonary exposure to nanosized CB and LPS caused lung inflammation without progression of atherosclerosis in ApoE-/- mice. Nevertheless, plasma extracted from mice exposed to nanosized CB induced vasoconstriction in aortas of naive wild-type mice, an effect possibly related to increased plasma serotonin.
Databáze: OpenAIRE