Studies on inflammation and wound healing: angiogenesis and collagen synthesis stimulated in vivo by resident and activated wound macrophages.
Studies on inflammation and wound healing: angiogenesis and collagen synthesis stimulated in vivo by resident and activated wound macrophages.
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DOI：
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发表时间：
1984-07
期刊：
影响因子：
3.8
通讯作者：
T. K. Hunt;D. Knighton;K. K. Thakral-K.;W. Goodson;W. Andrews
中科院分区：
文献类型：
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作者：
T. K. Hunt;D. Knighton;K. K. Thakral-K.;W. Goodson;W. Andrews
通过从兔皮下伤口的“死腔”中吸取液体，将伤口炎症细胞移植到角膜中，与合适的对照组相比，它们促进了愈合(即血管生成、纤维增生和新的胶原合成，从而形成了可见的、血管化的瘢痕组织)。对数据和文献的分析支持这样的结论：(1)炎症细胞控制着损伤消退后修复过程的持续；(2)巨噬细胞，而不是粒细胞，似乎是主要的贡献者；(3)巨噬细胞在伤口中的存在激活，释放刺激体内纤维增生、胶原合成和血管生成的物质；(4)组织损伤不是最大的修复刺激，因为内毒素治疗的巨噬细胞可以增强刺激胶原合成和血管生成的能力。提出了一种假说来解释损伤程度和修复程度之间臭名昭著的临床差异。
Wound inflammatory cells were harvested by aspiration of fluid from the "dead space" of subcutaneous rabbit wounds and transplanted into the cornea where, compared with suitable controls, they stimulated healing (i.e., angiogenesis, fibroplasia, and new collagen synthesis, which led to formation of visible, vascularized scar tissue). Analysis of the data and the literature supports the conclusions that: (1) inflammatory cells control the continuation of the repair process after the immediate effects of injury subside; (2) macrophages, as opposed to granulocytes, appear to be the major contributors; (3) activated by their presence in the wound, macrophages release substances that stimulate fibroplasia, collagen synthesis, and angiogenesis in vivo; and (4) tissue injury is not a maximum stimulus to repair, since endotoxin-treated macrophages have increased capacity to stimulate collagen synthesis and angiogenesis. A hypothesis is offered to explain the notorious clinical discrepancy between the extent of injury and the extent of repair.