Clin Res Cardiol (2021) DOI DOI https://doi.org/10.1007/s00392-021-01843-w

Vascular protection by ablation of lysozyme M-positive cells in a model of aircraft noise exposure

S. Steven1, K. Frenis1, J. Helmstädter1, S. Kalinovic1, S. Kröller-Schön1, M. T. Bayo Jimenez1, O. Hahad1, M. Oelze1, Y. Ruan2, S. Jiang2, P. Wenzel1, C. Sommer3, K. Frauenknecht3, A. Gericke2, A. Daiber1, T. Münzel1

1Zentrum für Kardiologie, Universitätsmedizin der Johannes Gutenberg-Universität Mainz, Mainz; 2Augenklinik, Universitätsmedizin Mainz, Mainz; 3Institut für Neuropathologie, Universitätsmedizin der Johannes Gutenberg-Universität Mainz, Mainz;

Objectives: Inflammation has been closely linked with the onset and exacerbation of a number of cardiovascular diseases including arterial hypertension. In addition, increases in inflammatory parameters have been correlated with noise as a cardiovascular risk factor. In the recent study we aimed to investigate the role of lysozyme M+ (LysM) myeloid cells in the vascular consequences following exposure to aircraft noise. Methods: Ablation of LysM+ cells was performed in LysMiDTR mice carrying an inducible cre promoter of the diphteria toxin receptor and a 10 days toxin treatment regimen. At the end of the treatment, animals were co-exposed to four days of noise at a maximum sound pressure level of 85 dB(A) and a mean sound pressure level of 72 dB(A). Flow cytometry analysis revealed increases in CD45+, CD11b+, F4/80+, and Ly6G−Ly6C+ extravasation into the aortas of noise-exposed mice, which was prevented by LysM+ cell ablation. LysM+ cells depletion led to normal value blood pressure after noise exposure. Further, endothelial function after noise exposure was improved in aorta and retinal arterioles. Correspondingly, phagocyte-derived reactive oxygen species in the aorta, heart, and retinal vessels were near control levels in ablated noise-exposed mice, complemented by reductions in phagocytic NADPH oxidase (NOX2), endothelial nitric oxide synthase (eNOS), and vascular cell adhesion molecule-1 (VCAM-1) mRNA in the aorta. The characteristic eNOS uncoupling occurring after noise exposure was partially prevented by LysM+ cell ablation.   Conclusion: These data point toward increased monocyte and macrophage response as key mediators in vascular dysfunction and arterial hypertension following noise exposure.

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