Adhesion molecules plasma levels

Kalfin, R., Righi, A., Del Rosso, A., Bagchi, D., Gererini, D., Cerinic, M., and Das, D., Activin, a grape seed-derived proanthocyanidin extract, reduces plasma levels of oxidative stress and adhesion molecules (ICAM-1, VCAM-1 and E-selectin) in systemic sclerosis. Free Radical Res., 36, 819,2002. 

G-CSF activates neutrophils, transforming them into cells capable of respiratory burst and release of secretory granules. It also modulates the expression of adhesion molecules on neutrophils as well as CD1 lb/CD18 and plasma elastase antigen levels. G-CSF induces proliferation of endothelial cells, phagocytic activity of neutrophils, reactive oxygen intermediate production by neutrophils and antibody-dependent cellular toxicity by neutrophils. 

Increases in plasma S-AA levels have previously been reported in patients with coronary disease (57). S-AA and plasma intracellular adhesion molecule-1 were elevated in patients with CAD and hyperhomocysteinemia, but only S-AA decreased after vitamin supplementation (35). Homocysteine activates nuclear factor- in endothelial cells, possibly via oxidative stress (58), and increases monocyte chemoattractant protein-1 expression in vascular smooth muscle cells (59). Additionally, it stimulates interleukin-8 expression in human endothelial cultures (60). These inflammatory factors are known to participate in the development of atherosclerosis. Taken together, these reports suggest an association of elevated tHcy and low-grade inflammation in CAD. 

MDD. Activation of some aspects of the immune system is generally associated with MDD, even in patients who are otherwise quite healthy. Many studies support this idea (Raison et al., 2006). Proinflammatory cytokines, such as IL-6 and TNF-a, are increased in plasma and in the CNS. There also are increases in the level of chemokines and adhesion molecules. 

CD56 (also known as neural cell adhesion molecule) is expressed on the cell surface of a number of different tissues including natural killer cells, glial and neurons. This antigen may be demonstrated on monocytic and myeloid leukemias, plasma cell dyscrasias, natural killer cell lesions, neural and astrocytic tumors as well as tumors with neuroendocrine differentiation. Antigen density on hematopoietic tumors tends to be at a lower level than on non-hematopoietic lesions and the validation with flow cytometry determination for this antigen is recommended. 

Inhibition by niacin of inflammatory and oxidative pathways may exert anti-atherosclerotic effects. In cultured human aortic endothelial cells, niacin increased cellular levels of nicotinamide adenine dinucleotide phosphate (reduced) (NADPH) and glutathione, regulators of redox reactions, and reduced production of reactive oxygen species. Niacin inhibited monocyte adhesion through the inhibition of tumour necrosis factor-alpha (TNF-a) induced expression of vascular cell adhesion molecule-1 (VCAM-1) and monocyte chemoattractant protein-1 (MCP-1) (Ganji et al. 2009). Persistent increases in plasma adiponectin, an adipokine with anti-inflammatory properties, were found after 6 months of niacin treatment in humans (Linke et al. 2009). 

Sickle erythrocytes have increased surface expression of CD36. Microvascular endothelial cells do express CD36. Adhesion between these CD36 molecules of the two cells types can be mediated via the bridging ligand thrombospondin". Indeed plasma thrombospondin levels are increased in SCA patients with pain crisis [15]. 

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