Cytokines and endothelial cell biology

Quantitation of Perivascular Monocytes and Macrophages around Cerebral Blood Vessels of Hypertensive and Aged Rats

“…In our previous studies, intracerebroventricular injection of lipopolysaccharide induced greater in creases in TNF-a activity in the CSF of hyperten sive and aged rats than in normotensive or young controls (Hallenbeck et ai., 1991;Siren et ai., 1992Siren et ai., , 1993. The present study extends these previous findings in that it suggests that the increased num bers of perivascular macrophages in hypertensive and aged rats could account for the enhanced pro duction of TNF-a in the brains of these rats, as monocytes and macrophages are a major source of TNF-a (Pober and Cotran, 1990). However, several other cell types in the CNS are capable of TNF-a expression.…”

“…Labeled monocytes and lymphocytes have been found in brain after in vivo labeling of the bone marrow (Roessman and Friede, 1968;Adrian, 1980, 1986;Wekerle et aI., 1986), and the blood-borne monocytes, in addi tion to the microglial cells, seem to contribute to the immune response in CNS injury (Roessman and Friede, 1968;Adrian, 1980, 1986;Ge hrmann et aI., 1992). Monocytes can adhere to, and penetrate across, brain endothelial cells via expres sion and binding of specific monocyte adhesion molecules to their specific adhesion molecule coun- terparts on endothelial cells (Pober and Cotran, 1990;Springer, 1990). In our previous studies, intracerebroventricular injection of lipopolysaccharide induced greater in creases in TNF-a activity in the CSF of hyperten sive and aged rats than in normotensive or young controls (Hallenbeck et ai., 1991;Siren et ai., 1992Siren et ai., , 1993.…”

“…The endothelial change involves, at a minimum, the expression of adhesion molecules that enable the monocytes to adhere to the vessel wall and undergo transendothelial migration in both large and small vessels, leading to local deposits of monocyte clusters in segments of the blood vessels. These monocyte clusters could then periodically signal the vessel endothelium via release of pro thrombotic, proinflammatory, and chemotactic me diators, such as TNF-a, IL-1, and perhaps platelet activating factor, to convert the endothelium to a procoagulant state and, in effect, prepare the vessel segments in a manner similar to the localized Shwartzman paradigm (Shwartzman, 1928;Movat , 1987;Hallenbeck et aI., 1988;Pober and Cotran, 1990). Complement activation or any stim ulus leading to activation of the coagulation system (including natural oscillation of coagulation poten tial, stress, infection, trauma, and inflammation) could then precipitate a localized reaction of the prepared vessel segment and lead to a local throm bosis or hemorrhage.…”

Human α‐enolase from endothelial cells as a target antigen of anti–endothelial cell antibody in Behçet's disease

“…Pretreatment of human endothelial cells with biologic response modifiers, such as interleukin-1␣ (IL-1␣) and tumor necrosis factor ␣ (TNF␣), leads to an increase in the expression of intercellular cell adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1, and E-selectin molecules and, consequently, to an increase in the adhesion of T lymphocytes (14,22). In a previous study, we found that AECA-positive sera from BD patients led to changes in the expression of adhesion molecules on the cell surface of HDMECs and promoted the adherence of T lymphocytes to HDMECs and, thus, initiated or amplified inflammatory vascular injury (10).…”

Plasma antioxidant vitamins and lipid peroxidation products in pregnancy induced hypertension

“…The unsaturated lipids and thiol containing proteins in cell membranes are susceptible to free radical attack. There are reports about increased free radical activity in PIH (2). But little is known about the part played by changes in specific antioxidants.…”