Burn injury reveals altered phenotype in mannan-binding lectin-deficient mice
Burn injury reveals altered phenotype in mannan-binding lectin-deficient mice
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DOI：
10.1038/sj.jid.5700748
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发表时间：
2007-06-01
影响因子：
6.5
通讯作者：
Takahashi, Kazue
中科院分区：
文献类型：
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作者：
Moller-Kristensen, Mette;Hamblin, Michael R.;Takahashi, Kazue
烧伤会破坏皮肤，皮肤是人体第二大天然免疫器官，并引发混乱的免疫和炎症反应。模式识别分子甘露聚糖结合凝集素(MBL)在宿主抵抗感染性病原体的一线防御中起着重要作用。MBL启动凝集素补体途径，发挥调理素的作用。最近的研究表明，MBL还调节炎症反应。我们报道MBL缺失型小鼠烧伤后的局部反应与野生型(WT)小鼠在下列重要生物学标志上有所不同：自发性焦痂分离、表皮和真皮变薄、可溶性因子上调，包括细胞因子、趋化因子、细胞黏附分子、生长因子结合蛋白和基质金属蛋白水解酶。缺乏C1q、C4或C3的小鼠在MBL零烧伤表型中没有表现出焦痂分离的缺乏。这些发现表明MBL是维持体内平衡的重要分子。
Burn injury destroys skin, the second largest innate immune organ in the body, and triggers chaotic immune and inflammatory responses. The pattern recognition molecule, mannan-binding lectin (MBL), plays an important role in the first-line host defense against infectious agents. MBL initiates the lectin complement pathway and acts as an opsonin. Recent studies suggest that MBL also modulates inflammatory responses. We report that local responses after burn in MBL null mice differ from those found in wild-type (WT) mice in the following important biological markers: spontaneous eschar separation, thinned epidermis and dermis, upregulation of soluble factors including cytokines, chemokines, cell adhesion molecules, a growth factorbinding protein, and matrix metal loprotei nases. Mice lacking C1q, C4, or C3 did not show the lack of eschar separation seen in MBL null-burn phenotype. These findings implicate MBL as an important molecule in the maintenance of the homeostatic balance.