Any science teacher, please assist! Need backing reading atherosclerosis?
Hi there. I've read nearly everything on atherosclerosis. I'm so confused as to why white blood cells can't fulfil their role in neutralising the cholestrol and other fatty materials at the sites of artery interrupt. Why do they just turn into foam cells and lie below the arteries? Is it some kind of chemical reaction that hinders their finction? Any info appreciated. I don't muse any websites will help, they are so complex, i just need a simple explanation so i can capture a basic grasp of what the problem is with these white blood cells :)
Answers:
Damaged tissue releases chemicals that attract white blood cell, which then attack microorganisms and consume damaged cells.
In atherosclerosis white blood cells—monocytes and lymphocytes—interact beside the endothelium, which is the cell layer of the blood vessel wall that faces the blood stream.
Following adherence of these white blood cells to the endothelium, they migrate across the endothelium and into the arterial wall. Once trapped contained by the arterial wall, the monocytes engorge oxidized (“bad”) cholesterol and are converted into fat-laden foam cells.
Formation and aggregation of foam cells is the first manifestation of atherosclerosis, leading to the narrowing of the vent of the artery and, eventually, to full-blown CVD.
Hope this makes it a bit clearer :)
The white blood cells (macrophages) almost become 'trapped' in the artery due to 'chemotactic cytokines' released by the oxidised LDLs already residing the artery wall. These 'chemotactic cytokines' are chemical messengers attracting the white cell to invade the artery and engulf the oxidised LDL, thereby initiating the atherosclerosis.
The oxidised LDL also generates adhesion molecules causing the white cells to stick to the blood vessel. The white cell when inside the blood vessel wall then uptake large amounts of oxidised LDL in an unregulated style because of the 'modified' nature of the oxidised LDL.
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Answers:
Damaged tissue releases chemicals that attract white blood cell, which then attack microorganisms and consume damaged cells.
In atherosclerosis white blood cells—monocytes and lymphocytes—interact beside the endothelium, which is the cell layer of the blood vessel wall that faces the blood stream.
Following adherence of these white blood cells to the endothelium, they migrate across the endothelium and into the arterial wall. Once trapped contained by the arterial wall, the monocytes engorge oxidized (“bad”) cholesterol and are converted into fat-laden foam cells.
Formation and aggregation of foam cells is the first manifestation of atherosclerosis, leading to the narrowing of the vent of the artery and, eventually, to full-blown CVD.
Hope this makes it a bit clearer :)
The white blood cells (macrophages) almost become 'trapped' in the artery due to 'chemotactic cytokines' released by the oxidised LDLs already residing the artery wall. These 'chemotactic cytokines' are chemical messengers attracting the white cell to invade the artery and engulf the oxidised LDL, thereby initiating the atherosclerosis.
The oxidised LDL also generates adhesion molecules causing the white cells to stick to the blood vessel. The white cell when inside the blood vessel wall then uptake large amounts of oxidised LDL in an unregulated style because of the 'modified' nature of the oxidised LDL.
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