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Authors: Frenis, Katie
Helmstädter, Johanna
Ruan, Yue
Schramm, Eva
Kalinovic, Sanela
Kröller-Schön, Swenja
Bayo Jimenez, Maria Teresa
Hahad, Omar
Oelze, Matthias
Jiang, Subao
Wenzel, Philip
Sommer, Clemens J.
Frauenknecht, Katrin B. M.
Waisman, Ari
Gericke, Adrian
Daiber, Andreas
Münzel, Thomas
Steven, Sebastian
Title: Ablation of lysozyme M-positive cells prevents aircraft noise-induced vascular damage without improving cerebral side effects
Online publication date: 4-Aug-2022
Language: english
Abstract: Aircraft noise induces vascular and cerebral inflammation and oxidative stress causing hypertension and cardiovascular/cerebral dysfunction. With the present studies, we sought to determine the role of myeloid cells in the vascular vs. cerebral consequences of exposure to aircraft noise. Toxin-mediated ablation of lysozyme M+ (LysM+) myeloid cells was performed in LysMCreiDTR mice carrying a cre-inducible diphtheria toxin receptor. In the last 4d of toxin treatment, the animals were exposed to noise at maximum and mean sound pressure levels of 85 and 72 dB(A), respectively. Flow cytometry analysis revealed accumulation of CD45+, CD11b+, F4/80+, and Ly6G−Ly6C+ cells in the aortas of noise-exposed mice, which was prevented by LysM+ cell ablation in the periphery, whereas brain infiltrates were even exacerbated upon ablation. Aircraft noise-induced increases in blood pressure and endothelial dysfunction of the aorta and retinal/mesenteric arterioles were almost completely normalized by ablation. Correspondingly, reactive oxygen species in the aorta, heart, and retinal/mesenteric vessels were attenuated in ablated noise-exposed mice, while microglial activation and abundance in the brain was greatly increased. Expression of phagocytic NADPH oxidase (NOX-2) and vascular cell adhesion molecule-1 (VCAM-1) mRNA in the aorta was reduced, while NFκB signaling appeared to be activated in the brain upon ablation. In sum, we show dissociation of cerebral and peripheral inflammatory reactions in response to aircraft noise after LysM+ cell ablation, wherein peripheral myeloid inflammatory cells represent a dominant part of the pathomechanism for noise stress-induced cardiovascular effects and their central nervous counterparts, microglia, as key mediators in stress responses.
DDC: 610 Medizin
610 Medical sciences
Institution: Johannes Gutenberg-Universität Mainz
Department: FB 04 Medizin
Place: Mainz
Version: Published version
Publication type: Zeitschriftenaufsatz
License: CC BY
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Journal: Basic research in cardiology
Pages or article number: 31
Publisher: Steinkopff
Publisher place: Darmstadt u.a.
Issue date: 2021
ISSN: 1435-1803
Publisher DOI: 10.1007/s00395-021-00869-5
Appears in collections:JGU-Publikationen

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