Vascular cell adhesion molecules chemokines

During the generation of functional lymphoid tissue organizers, LT-pR signaling leads to expression of mucosal addressin cell adhesion molecule (MAdCAM-1), intercellular adhesion molecule 1 (ICAM-1), and vascular cell-adhesion molecule 1 (VCAM-1) on endothelial cells, as well as the production of the chemokines CXCL13, CCL19, and CCL21 by stromal cells and HEVs (Carlsen et al., 2005). 

NF-kB regulates many genes involved in inflammation, such as inducible nitric oxide synthase (iNOS), proinflammatory cytokines, IL-1, mmor necrosis factor-alpha (TNF-a), IL-6, chemokine, IL-8, E-selectin, vascular cell adhesion molecule 1 (ICAM-1), and granulocyte-macrophage colony stimulating factor (GM-CSF) (Brennan et al., 1995 Akira and Kishimoto, 1997 Bames and Adcock, 1998 Rahman and MacNee, 1998 McClintock et al., 2002). Arroyo et al. (2000) found a dose-dependent increase in TNF-a, IL-6, and interleukin-1-beta (IL-1-beta) in SM-treated human keratinocyte cells. 

OTHER CYTOKINES ENDOTHELIAL DERIVED CHEMOKINES INTRACELLULAR ADHESION MOLECULES (ICAM) VASCULAR CELL ADHESION MOLECULES (VCAM) MONOCYTE CtX.C JY STIMULATING FACTOR (MCSF) MONOCYTE CHEMOATTRACTANT FACTOR-1 (MCP -1) SELECTINS... 

There are multicellular interactions that are important in inflammatory processes and in vascular remodeling. Activated platelets induce endothelial cells to secrete chemokines and to express adhesion molecules, indicating that platelets could initiate an inflammatory (Table I) response of the vessel wall. Activated platelets promote leukocyte binding to inflamed or atherosclerotic lesions (27,28). Cell adhesion molecules (CAMs) are responsible for leukocyte-endothelium interactions. It plays a crucial role in inflammation and atherogenesis. Vascular CAM-1 (VCAM-I)and intracellular CAM-1 (ICAM-I) promote monocyte recruitment to sites of injury and constitute a critical step in inflammation and in atherosclerotic plaque development. TSP-1, a matricellular protein released in abundance from activated platelets and accumulated in sites of vascular injury, induces the expression of VCAM-1 and ICAM-1 on endothelium and significantly increases the monocyte attachment (29). 

Frequently, the EAR is followed by a late phase response 4-6 h later and it is caused by the pulmonary sequestration of eosinophils, neutrophils, mast cells, and T-lymphocytes. This leukocyte recruitment depends on mast cell-derived mediators such as TNFa and various chemokines, as well as on the expression of adhesion molecules on leukocytes (e.g. VLA-4, CD11/18) and vascular endothelial cells (e.g. VCAM-1, ICAM-1, E-selectin). Products of these leukocytes have several functions First, they cause the second phase of bron-choconstriction, mucus secretion, and airway swelling second, they cause tissue destruction third, they launch and entertain the chronic inflammation. 

The vascular endothelium plays an important role in regulation of vascular tone and permeability. Dilatation of arterioles to increase blood flow and constriction of endothelial cells of postcapillary venules causing exsudation of plasma constituents illustrates the complex nature of this cell type. Moreover, by expression of adhesion molecules and secretion of chemokines endothelial cells play an important role in the recruitment of leukocytes to the inflamed area. Endothelial cells express two basic types of adhesion molecules on their surface ... 

Initial attempts at treating or preventing restenosis focused primarily on inhibition of the proliferation of vascular SMCs (VSMCs). A series of agents successful at inhibition of SMC proliferation in vitro as well as in vivo in animal models such as carotid injury models in the rat failed to demonstrate benefit in the clinic. More recently, it has been shown in addition to effects on SMCs, that mechanical intervention also activates the recruitment and activation of immune cells. Cell signaling through cytokines, chemokines, and adhesion molecule expression results in the recruitment to the vascular wall of cells of many types, as well as their proliferation, migration, and/or maturation. 

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