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Deposition of complement C3 and factor H in tissue traumatized by burn injury.

机译:在烧伤引起的组织中补体C3和H因子的沉积。

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Activation of complement is known to accompany burn injury. To study deposition of complement proteins within tissue traumatized by burn we employed the technique of intravital microscopy using a murine dorsal skinfold chamber model. C3, factor H, factor B, HSA, and transferrin were labeled fluorescently and injected into the tail vein of mice which had been subjected to a small third degree burn within the skin fold. Only C3 and factor H deposited within blood vessels of the traumatized tissue. Binding was specific because it occurred only in and proximal to burn sites, and neither C3 nor factor H was observed to accumulate in blood vessels of healthy tissue. Furthermore, fluorescently labelled HSA, factor B, and transferrin all failed to deposit at or around burn loci. The deposition of C3 and factor H occurred within 10 min of injury and was intravascular occurring in major blood vessels, capillaries, and post-capillary venules, with little evidence of accumulation in the interstitium. Since both C3 fragments and factor H are recognized as adhesion molecules by granulocyte receptors, these deposited proteins could promote leukocyte accumulation, thereby contributing to an initiation of an inflammatory cascade at a site of burn injury.
机译:已知补体的激活伴随着烧伤。为了研究补体蛋白在烧伤创伤组织内的沉积,我们使用了鼠背皮褶腔模型的活体显微镜技术。将C3,H因子,B因子,HSA和转铁蛋白进行荧光标记,并注入已在皮肤褶皱内遭受三度小烧伤的小鼠尾静脉中。仅C3和因子H沉积在受创组织的血管内。结合是特异性的,因为它仅发生在烧伤部位及其附近,并且没有观察到C3和H因子在健康组织的血管中积聚。此外,荧光标记的HSA,B因子和转铁蛋白均未沉积在烧伤位点处或周围。 C3和H因子的沉积发生在损伤后10分钟之内,并且在血管内发生在主要血管,毛细血管和毛细血管后小静脉中,几乎没有在间质中积累的证据。由于C3片段和H因子均被粒细胞受体识别为粘附分子,因此这些沉积的蛋白质可促进白细胞积聚,从而有助于在烧伤部位引发炎症级联反应。

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