The McComb Research Foundation, Royal Perth Hospital, Perth, WA, Australia.
Burns. 2009 May;35(3):356-64. doi: 10.1016/j.burns.2008.07.011. Epub 2008 Oct 25.
Scarring after severe burn is a result of changes in collagen deposition and fibroblast activity that result in repaired but not regenerated tissue. Re-epithelialisation of wounds and dermal cell repopulation has been thought to be driven by cells in the periphery of the wound. However, recent research demonstrated that cells originating from the bone marrow contribute to healing wounds in other tissues and also after incisional injury. We investigated the contribution of bone marrow-derived cells to long-term cell populations in scar tissue (primarily fibroblasts and keratinocytes) after severe burn. Wild-type mice were lethally irradiated and then the bone marrow reconstituted by injection of chimeric bone marrow cells expressing EGFP marker protein. Mice with chimeric bone marrow were then given a burn, either an 1-cm diameter injury (to mimic minor injury) or 2-cm diameter (to mimic moderate injury). Wounds were analysed at days 1, 3, 7, 14, 21, 28, 56 and 120 using FACS and immunohistochemistry to identify the percentage and cell type within the wound originating from the bone marrow. The inflammatory cell infiltrate at the early time-points was bone marrow in origin. At later time-points, we noted that over half of the fibroblast population was bone marrow-derived; we also observed that a small percentage of keratinocytes appeared to be bone marrow in origin. These findings support the theory that the bone marrow plays an important role in providing cells not only for inflammation but also dermal and epidermal cells during burn wound healing. This increases our understanding of cell origins in the healing wound, and has the potential to impact on clinical practice providing a potential mechanism for intervention away from conventional topical treatments and directed instead to systemic treatments affecting the bone marrow response.
严重烧伤后的瘢痕形成是胶原沉积和成纤维细胞活性变化的结果，导致修复但未再生的组织。人们一直认为，伤口的再上皮化和真皮细胞再填充是由伤口周围的细胞驱动的。然而，最近的研究表明，骨髓来源的细胞有助于其他组织和切口损伤后的伤口愈合。我们研究了骨髓源性细胞对严重烧伤后瘢痕组织（主要是成纤维细胞和角蛋白细胞）中长期细胞群体的贡献。野生型小鼠接受致死性辐射，然后通过注射表达 EGFP 标记蛋白的嵌合骨髓细胞进行骨髓重建。嵌合骨髓小鼠随后接受 1cm 直径的损伤（模拟小损伤）或 2cm 直径的损伤（模拟中度损伤）。使用 FACS 和免疫组织化学分析在第 1、3、7、14、21、28、56 和 120 天的伤口，以鉴定源自骨髓的伤口内细胞百分比和细胞类型。在早期时间点，炎症细胞浸润来自骨髓。在后期时间点，我们注意到超过一半的成纤维细胞群体来自骨髓；我们还观察到一小部分角蛋白细胞似乎来自骨髓。这些发现支持了骨髓在提供细胞方面发挥重要作用的理论，不仅在炎症期间，而且在烧伤伤口愈合过程中也为真皮和表皮细胞提供细胞。这增加了我们对愈合伤口中细胞起源的理解，并有可能对临床实践产生影响，为干预提供潜在的机制，远离传统的局部治疗，转而针对影响骨髓反应的系统治疗。
