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macrophages

CRP–Mediated Low Density Lipoprotein Uptake by Macrophages – (03-22-01)

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CRP–Mediated Low Density Lipoprotein Uptake by Macrophages

I may need to clarify what this article is talking about. First, it is current theory that macrophages become foam cells once they take up LDL cholesterol from the bloodstream. These foam cells are what lead to the buildup of plaque on the arteries. This article is suggesting that CRP (a marker of chronic inflammation) increases the attraction (“opsonizes”) between the LDL and the macrophages. Low level chronic inflammation can come from so many different sources; and can in turn lead to a multitude of chronic diseases.

Circulation — Abstracts: Zwaka et al. 103 (9): 1194

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Vitamin E protects cholesterol from damage – (05-03-01)

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α-Tocopherol decreases CD36 expression in macrophages

I know this title seems confusing, but in general it supports previous research on Vit E preventing the damage caused by high cholesterol levels. Remember–high cholesterol can not damage the body until it itself is damaged. Antioxidant therapy should be an instrumental aspect of any therapy aimed at lowering cholesterol. A little note here—the tocopherols (in which Vit E belongs) is actually a group of numerous types. The highest quality supplements will contain mixed tocopherols to best mimic nature.

J. Lipid Res. — Abstracts: Devaraj et al. 42 (4): 521

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INHIBITION OF NF-KAPPAB SUPPRESSES IMMUNE RESPONSE – (11-03-03)

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Inhibition of NF-kappaB activation in macrophages increases atherosclerosis in LDL receptor–deficient mice

Here is yet another example of how complex the human body is and how screwing with physiology can lead to unexpected consequences. NF-kappaB is an upstream control substance that turns on many other aspects of the immune system, including TNF-alpha.

This study finds that inhibition of NF-kappaB, thus suppressing the immune response, leads to INCREASED atherosclerosis in mice. If this is the case, what might the long term side effects of TNF alpha suppression in rheumatoid arthritis and Crohn’s be doing to a patient’s blood vessels??

JCI — Abstracts: Kanters et al. 112 (8): 1176.

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MECHANISM UNDERLYING OXIDATIVE STRESS – 05-01-05)

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Mechanism underlying oxidative stress-mediated lipotoxicity

In a nutshell, the researchers in this study found that elevated triglycerides (as would be found in insulin resistance) get sucked up into the macrophages (a type of white blood cells), and once there, started to destroy the mitochondria of the cell resulting in cell death.  The death of a macrophage in the bloodstream can lead to the production of foam cells and subsequent plague in the arteries.

Interestingly, vit C, NAC and resveratrol protected the macrophages from this death.  So, to extrapolate into a living, breathing human, antioxidants protect the cells that produce plaquing in the arteries, resulting in less plaque.

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