13 February 2008
question
Hi class. I was just wondering how ischemia causes damage to the blood brain barrier, which in turn allows leukocytes and neutrophils access to the infarction site. I understand how the microglia change metabolically and chemically to become phagocytic during ischemia; does this possible have something to do with the breakdown of the B.B.B. at the site?
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Hey, we talked a little about this in class today, but in case anyone else was curious I looked back at the paper, “The inflammatory Response in Stroke,” and in section 4.2, it mentions the role chemokines play during ischemia. It states that chemokines work as chemoattractants for inflammatory cells, while at the same time increasing the permeability of the blood brain barrier (BBB). The endothelial cells of the blood capillaries in the brain are strongly bound to each other with tight junctions, preventing entry of (among other things) inflammatory cells into the brain. But when the chemokine MCP-1 (monocyte chemoattractant protein-1) was added to an in vitro BBB model, the tight junction proteins were altered, allowing gaps to open between endothelial cells, increasing the permeability substantially. Section 2.3 mentions that astrocytes, when activated during stroke, can produce chemokines, as well as other inflammation mediators. So, I think that an increase in chemokine release by activated astrocytes could promote the opening of the BBB, allowing the recruitment and entry of inflammatory cells into the brain, causing further damage.
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