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Roth, S.* ; Singh, V.K.* ; Tiedt, S.* ; Schindler, L.* ; Huber, G. ; Geerlof, A. ; Antoine, D.J.* ; Anfray, A.* ; Orset, C.* ; Gauberti, M.* ; Fournier, A.* ; Holdt, L.M.* ; Harris, H.E.* ; Engelhardt, B.* ; Bianchi, M.E.* ; Vivien, D.* ; Haffner, C.* ; Bernhagen, J.* ; Dichgans, M.* ; Liesz, A.*

Brain-released alarmins and stress response synergize in accelerating atherosclerosis progression after stroke.

Sci. Transl. Med. 10:eaao1313 (2018)

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Stroke induces a multiphasic systemic immune response, but the consequences of this response on atherosclerosis-a major source of recurrent vascular events-have not been thoroughly investigated. We show that stroke exacerbates atheroprogression via alarmin-mediated propagation of vascular inflammation. The prototypic brain-released alarmin high-mobility group box 1 protein induced monocyte and endothelial activation via the receptor for advanced glycation end products (RAGE)-signaling cascade and increased plaque load and vulnerability. Recruitment of activated monocytes via the CC-chemokine ligand 2-CC-chemokine receptor type 2 pathway was critical in stroke-induced vascular inflammation. Neutralization of circulating alarmins or knockdown of RAGE attenuated atheroprogression. Blockage of. 3-adrenoreceptors attenuated the egress of myeloid monocytes after stroke, whereas neutralization of circulating alarmins was required to reduce systemic monocyte activation and aortic invasion. Our findings identify a synergistic effect of the sympathetic stress response and alarmin-driven inflammation via RAGE as a critical mechanism of exacerbated atheroprogression after stroke.

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