Brain leukocytes infiltrating

Marcheselh, V. L., Hong, S., Lukiw, W. J. et al. Novel docosanoids inhibit brain ischema-reperfusion-mediated leukocyte infiltration and pro-inflammatory gene expression. J. Biol. Chem. 278,43807-43817,2003. 

Human CEC cultured on filter inserts can be used to measure brain penetration of drugs to make in vitro-in vivo correlations. They can further be used to study for example brain inflammation that has been implicated in the development of brain edema and secondary brain damage in ischemia and trauma. Zhang et al. (2000) studied leukocyte infiltration across the blood-brain barrier and showed the expression of adhesion molecules and leukocyte chemoattractants under ishemia in vitro conditions. 

Novel docosanoids inhibit brain ischemia-reperfusion-mediated 137. leukocyte infiltration and pro-inflammatory gene expression. J. 

Leukocyte infiltration across the blood brain bariier after ischemic stroke is dependent on the expression of adhesion molecules on leukocytes and endothelial cells. 

Inflammatory cells infiltrating postischemic tissue are considered to contribute to disability after cerebral ischemia [5,8,17]. Identification of factors involved in the selective recruitment and accumulation of inflammatory cells into ischemic brain tissue and the mechanisms behind the entry of leukocytes through the blood-brain barrier into sites of ischemia are not completely understood [5,8]. Locally produced proinflammatory cytokines such as TNF-a, IL-1 P, and IL-6 initiate the inflammatory process. TNF-a and IL-1 P mRNA elevate in the brain after experimental middle cerebral artery occlusion [5,51,81]. While, IL-1 p and TNF-a play a major role in promoting adhesion between endothelial cells and leukocytes, they are poor attractants for polymorphonuclear leukocytes and monocytes [7]. Astrocytes and endothelial cells can respond in vitro to such proinflammatory cytokines with enhanced expression of chemokines, which results in the influx of leukocytes to areas of inflammation [5,8,103]. 

Stroke-related inflammation in the brain appears to largely result from a selective migration and infiltration of systemic (i.e., circulating) leukocytes to the focus of cerebral ischemia. These cells are predominantly those of the innate immune system, at least initially. Activated neutrophil polymorphs begin to infiltrate as early as 4h after stroke, initially being... 

This may change during neurodegenerative disease and associated neuroinflammation, where the isolating capacity of the blood-brain barrier deteriorates and thus allows the infiltration of blood leukocytes. The increased permeability of the blood-brain barrier is the result ofthe disruption of tight junctional structures as well... 

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