Adventitial lymphatic capillary expansion impacts on plaque T cell accumulation in atherosclerosis.

During plaque progression, inflammatory cells progressively accumulate in the adventitia, paralleled by an increased presence of leaky vasa vasorum. We here show that next to vasa vasorum, also the adventitial lymphatic capillary bed is expanding during plaque development in humans and mouse models of atherosclerosis. Furthermore, we investigated the role of lymphatics in atherosclerosis progression.

Interleukin 23 levels are increased in carotid atherosclerosis: possible role for the interleukin 23/interleukin 17 axis.

Background And Purpose: Interleukin (IL)-23 is a cytokine in the IL-12 family, mainly produced by antigen-presenting cells with a central role in inflammation. We hypothesize that IL-23 is also important in atherogenesis and investigate this in a population with carotid atherosclerosis.

Methods: Plasma levels of IL-23 were measured in patients with carotid artery stenosis and in healthy controls.

CXCR4 blockade induces atherosclerosis by affecting neutrophil function.

Aims: The SDF-1α/CXCR4 dyad was previously shown by us and others to be instrumental in intimal hyperplasia as well as early stage atherosclerosis. We here sought to investigate its impact on clinically relevant stages of atherosclerosis in mouse and man.

Methods And Results: Immunohistochemical analysis of CXCR4 expression in human atherosclerotic lesions revealed a progressive accumulation of CXCR4(+) cells during plaque progression.

Increased levels of the homeostatic chemokine CXCL13 in human atherosclerosis - Potential role in plaque stabilization.

Objectives: Based on the newly recognized role of the homeostatic chemokines in inflammation, we hypothesized that CXCL13 could modulate atherogenesis and plaque destabilization.

Methods: The study included in vivo analyses in patients with carotid atherosclerosis and in vitro experiments in cells involved in atherogenesis (ie, monocytes/macrophages, vascular smooth muscle cells [SMC], and platelets).

Results: Our main findings were: (i) Patients with carotid atherosclerosis (n = 130) had increased plasma levels of CXCL13 with particularly high levels in symptomatic disease.

Plasmacytoid dendritic cells protect against atherosclerosis by tuning T-cell proliferation and activity.

Rationale: Unlike conventional dendritic cells, plasmacytoid DCs (PDC) are poor in antigen presentation and critical for type I interferon response. Though proposed to be present in human atherosclerotic lesions, their role in atherosclerosis remains elusive.

Objective: To investigate the role of PDC in atherosclerosis.

Chemokines as therapeutic targets for atherosclerotic plaque destabilization and rupture.

Chemokines are instrumental in the initiation and progression of atherosclerosis. Recent advances in genomic technologies and the recognition of atherosclerosis as an inflammatory disease have given great impetus to studies addressing the relevance of chemokines for the clinically manifest stages of atherosclerosis and acute cardiovascular syndromes. In this paper, we will review the current status of these studies, highlighting those chemokines that have already been associated with plaque destabilization and rupture.

Intestinal cytoskeleton degradation precedes tight junction loss following hemorrhagic shock.

Hemorrhagic shock (HS) leads to intestinal barrier loss, causing systemic inflammation, which in turn can ultimately lead to multiorgan dysfunction syndrome. Barrier function is based on tight junctions (TJs) between intact epithelial cells. These TJs are anchored in the cell via the filamentous actin (F-actin) cytoskeleton.