The inflammatory response in extravasated leukocytes in patients with coronary artery disease

摘要: Coronary artery disease (CAD) is a manifestation of chronic inflammation in the coronary arteries. The inflammatory process results accumulation monocyte derived cells and formation atherosclerotic plaques intima vessel wall. Neutrophils are mainly associated with ruptured precise role CAD not fully known. Extravasation into local sites coordinated by adhesion molecules chemokines transforms leukocytes activated tissue dwelling cells. aim this thesis was to investigate extravasated monocytes neutrophils patients stable CAD. A skin chamber method applied order induce from which were collected. Paper I II describes monocytes. Patients had similar number exudate compared healthy subjects. expression CD11b following extravasation lower controls. This might result an increased retention at site. Other markers extravasation, VLA-4 CX3CR1, altered. Extravasated further analyzed for functional alterations. Markers antigen presentation, HLA-DR CD86, binding modified cholesterol, CD36 scavenger receptor A1 (SR-A1) circulation. Furthermore, acetylated low density lipoprotein (acLDL) extravasation. Monocytes controls response. However, fluid enhanced vitro stimulation mononuclear III IV neutrophils. significantly production reactive oxygen species (ROS) indicate refractory stage gene assessed array. general induction IL-1 axis seen chemokines. Expression IL-1R on human confirmed flow cytometry electron microscopy resulted CCL CXCL chemokine protein expressions. Compared controls, expressions CCL20 CXCL2. finding indicates that may have immuno-modulatory profile could enhance pathological processes atherosclerosis. major findings potential mechanism entrapment sites. In addition, milieu be pro-atherosclerotic. altered responsiveness refractory. alter