Adherence of neutrophils to cultured human microvascular endothelial cells. Stimulation by chemotactic peptides and lipid mediators and dependence upon the Mac-1, LFA-1, p150,95 glycoprotein family
Article Abstract:
The inflammatory response (inflammation) is an attempt by the body to isolate an area affected by injury or destruction of tissues by chemical, immunologic or other factors. The area is walled off by a tissue reaction which is characterized by four factors: swelling, redness, pain and increased temperature. On a microscopic level white blood cells (particularly neutrophils) invade the area by passing through small blood vessel walls. Blood flow to the area increases, leading to redness and higher temperature. The walls of vessels become more permeable and a fluid accumulation produces swelling and pain. One of the earliest events in the inflammatory process is the invasion of circulating white blood cells. Neutrophils adhere to (and even pass through) the walls of vessels, adding to the distress. Although these factors are well known, the molecular events which trigger them are not yet clear. These experiments explore the relationship of the inflammatory reactions to the association of certain cellular mediators and surface glycoproteins (receptors) on the white blood cells. (Receptors are molecular structures either within a cell or on its surface which act as binding sites for a single type of molecule, and act in some manner as a trigger of physiologic events.) This study employs tissue cultures (a technique for growing human or animal cells inside an incubator, usually in a liquid medium which approximates tissue fluid. Using cultures allows investigators to directly observe the effect of chemical and cell interactions.) The authors show that certain peptides (the building blocks of proteins), fat-mediating substances and activators of platelet activity (platelets are small fragments of cells involved in clotting) affect the ability of these cells to adhere. The mechanism of action appears to be the ability of the experimental agents to induce the neutrophil to produce small glycoproteins on its surface membranes which may act as surface receptors. Cells from patients which suffered from known adhesion deficiency failed to become stimulated by the various factors, presumably because they lacked this ability.
Publication Name: Journal of Clinical Investigation
Subject: Health care industry
ISSN: 0021-9738
Year: 1989
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Mechanism of mitogen-induced stimulation of glucose transport in human peripheral blood mononuclear cells. Evidence of an intracellular reserve pool of glucose carriers and their recruitment
Article Abstract:
The study examines the effect of phytohemagglutinin, a compound which causes an increase in cell division, on a specific population of white blood cells. The ability of these cells to transport glucose and utilize glucose is affected by the compound. Data suggest that there are two types of transport mechanisms for glucose in these cells and that treatment with phytohemagglutinin causes such "transporters" to migrate from the internal area to the surface membrane of these white blood cells where they are active. At the surface membrane this compound accounts for 60 percent of the increase in the ability to transport glucose.
Publication Name: Journal of Clinical Investigation
Subject: Health care industry
ISSN: 0021-9738
Year: 1989
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Intracellular pH during "chemical hypoxia" in cultured rat hepatocytes. Protection by intracellular acidosis against the onset of cell death
Article Abstract:
The study explores the effect of decreased oxygen in growing rat liver cells in the laboratory. The liver cells were poisoned by chemical treatment and were measured. Following poisoning the pH inside the cells remained acidic for 30-40 minutes before they became basic and cell death occurred. The authors conclude that the retention of acidic conditions within cells was a protective mechanism against liver cell death following the poisoning. This may represent a general mechanism that works to protect cells against decreased blood flow and decreased local oxygen supply.
Publication Name: Journal of Clinical Investigation
Subject: Health care industry
ISSN: 0021-9738
Year: 1989
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