Publications by authors named "Andreas Giraud"
The triggering receptor expressed on myeloid cells 1 (TREM-1) drives inflammatory responses in several cardiovascular diseases but its role in abdominal aortic aneurysm (AAA) remains unknown. Our objective was to explore the role of TREM-1 in a mouse model of angiotensin II-induced (AngII-induced) AAA. TREM-1 expression was detected in mouse aortic aneurysm and colocalized with macrophages.
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- Adaptive immune responses play a role in the development of atherosclerosis, with type 1 responses being harmful and type 2 responses providing protection.
- The study focused on thymic stromal lymphopoietin (TSLP), a cytokine important for type 2 immune responses, to see if it was crucial for the anti-atherogenic effects of Freund's adjuvant.
- Results showed that Freund's adjuvant induced TSLP expression through different mechanisms in male and female mice, and TSLP signaling was essential for reducing atherosclerosis, as ApoE mice had less atherogenesis compared to ApoE/TSLPR mice that lacked this signaling.
Selective EGFR (Epidermal Growth Factor Receptor) Deletion in Myeloid Cells Limits Atherosclerosis-Brief Report.
Arterioscler Thromb Vasc Biol
January 2018
Article Synopsis
- The study investigates the effects of inhibiting EGFR in myeloid cells on the development of atherosclerosis.
- Results showed that irradiated mice with specific bone marrow reconstitution had significantly smaller atherosclerotic lesions after a high-fat diet, indicating less macrophage accumulation and necrotic core size.
- The deletion of EGFR in these cells led to reduced production of pro-inflammatory cytokines TNF-α and IL-6, less lipid uptake by macrophages, and ultimately a decrease in atherosclerosis progression.
Rationale: Chronic inflammation is central in the development of atherosclerosis. Both innate and adaptive immunities are involved. Although several studies have evaluated the functions of natural killer (NK) cells in experimental animal models of atherosclerosis, it is not yet clear whether NK cells behave as protective or proatherogenic effectors.
View Article and Find Full Text PDFAngiotensin II (AngII) promotes hypertension, atherogenesis, vascular aneurysm and impairs post-ischemic cardiac remodeling through concerted roles on vascular cells, monocytes and T lymphocytes. However, the role of AngII in B lymphocyte responses is largely unexplored. Here, we show that chronic B cell depletion (Baffr deficiency) significantly reduces atherosclerosis in Apoe mice infused with AngII.
View Article and Find Full Text PDFRationale: Necrotic core formation during the development of atherosclerosis is associated with a chronic inflammatory response and promotes accelerated plaque development and instability. However, the molecular links between necrosis and the development of atherosclerosis are not completely understood. Clec9a (C-type lectin receptor) or DNGR-1 (dendritic cell NK lectin group receptor-1) is preferentially expressed by the CD8α subset of dendritic cells (CD8α DCs) and is involved in sensing necrotic cells.
View Article and Find Full Text PDFAims: Abdominal aortic aneurysm (AAA), frequently diagnosed in old patients, is characterized by chronic inflammation, vascular cell apoptosis and metalloproteinase-mediated extracellular matrix destruction. Despite improvement in the understanding of the pathophysiology of aortic aneurysm, no pharmacological treatment is yet available to limit dilatation and/or rupture. We previously reported that human gingival fibroblasts (GFs) can reduce carotid artery dilatation in a rabbit model of elastase-induced aneurysm.
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