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 |
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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 |
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