Toll-like receptor 4 signaling regulates the acute local inflammatory response to injury and the fibrosis/neovascularization of sterile wounds.
Toll-like receptor 4 signaling regulates the acute local inflammatory response to injury and the fibrosis/neovascularization of sterile wounds.
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DOI：
10.1111/wrr.12061
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发表时间：
2013-07
期刊：
影响因子：
--
通讯作者：
Albina JE
中科院分区：
文献类型：
--
作者：
Brancato SK;Thomay AA;Daley JM;Crane MJ;Reichner JS;Sabo E;Albina JE
在TLR4信号缺失（C3H/HeJ或TLR4−/−）和对照组小鼠中，采用皮下植入聚乙乙醇海绵创面模型，研究toll样受体4 （TLR4）在无菌创面炎症和纤维化中的调控作用。C3H/HeJ和C3H/HeOuJ动物损伤后1、3和7天的总和差异伤口细胞计数无差异。两种菌株的血液单核细胞表达CCR2相同。与对照组相比，C3H/HeJ小鼠第一天伤口中含有较少的gr -1高水平伤口巨噬细胞、CCL3和CCL5，以及更多的CCL17。伤口液中CCL2、CX3CL1、肿瘤坏死因子-α、白细胞介素(IL)-6、IL-10、IL-12和干扰素-γ的积累不依赖于TLR4。C3H/HeJ和C3H/HeOuJ小鼠的伤口巨噬细胞表达CCR4和CCR5，但不表达CCR1和CCR3。在CCR5−/−小鼠或C3H/HeOuJ动物中注射中和性抗ccl3和抗ccl5抗体后，伤口巨噬细胞募集未发生改变。在C3H/HeJ小鼠中中和CCR4配体CCL17不会改变伤口巨噬细胞的数量。与C3H/HeOuJ小鼠相比，C3H/HeJ小鼠21天创面胶原含量和新生血管数量增加了两倍。伤后7天和21天各组间肌成纤维细胞数量无明显差异。HeJ小鼠伤口纤维化和血管生成的增加与伤口液中转化生长因子-β和成纤维细胞生长因子2的浓度升高有关。伤口液不含可检测到的脂多糖，也不诱导J774的i - κ b α降解。A1巨噬细胞。结果支持内源性TLR4配体在无菌伤口炎症和修复中的调节作用。
The role of Toll-like receptor 4 (TLR4) in the regulation of inflammation and fibrosis in sterile wounds was investigated in TLR4 signal-deficient (C3H/HeJ or TLR4−/−) and control mice using the subcutaneously implanted polyvinyl alcohol sponge wound model. Total and differential wound cell counts 1, 3, and 7 days after injury did not differ between C3H/HeJ and C3H/HeOuJ animals. Blood monocytes from both strains expressed CCR2 equally. Day one wounds in C3H/HeJ mice contained fewer Gr-1high wound macrophages, CCL3, and CCL5, and more CCL17 than those in controls. The accumulation of CCL2, CX3CL1, tumor necrosis factor-α, interleukin (IL)-6, IL-10, IL-12, and interferon-γ in wound fluids was not TLR4 dependent. Wound macrophages from C3H/HeJ and C3H/HeOuJ mice expressed CCR4 and CCR5, but not CCR1 or CCR3. Wound macrophage recruitment was not altered in CCR5−/− mice or in C3H/HeOuJ animals injected with neutralizing anti-CCL3 and anti-CCL5 antibodies. Neutralization of the CCR4 ligand CCL17 in C3H/HeJ mice did not alter wound macrophage populations. There was a twofold increase in collagen content and number of neovessels in 21-day-old wounds in C3H/HeJ vs. C3H/HeOuJ mice. There were no differences between strains in the number of myofibroblasts in the wounds 7 or 21 days post-wounding. The increased fibrosis and angiogenesis in wounds from /HeJ mice correlated with higher concentrations of transforming growth factor-β and fibroblast growth factor 2 in wound fluids from these animals. Wound fluids did not contain detectable lipopolysaccharide and did not induce IκBα degradation in J774.A1 macrophages. Results support a role for endogenous ligands of TLR4 in the regulation of inflammation and repair in sterile wounds.
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影响因子：
--
作者：
Grote K;Schütt H;Schieffer B
通讯作者：
Schieffer B
影响因子：
4.8
作者：
Okamura, Y;Watari, M;Strauss, JF
通讯作者：
Strauss, JF
TLR4 活性是解决急性和慢性肺损伤后肺部炎症和纤维化所必需的
影响因子：
6
作者：
Yang, Hong-Zhen;Wang, Jia-Ping;Hu, Zhuo-Wei
通讯作者：
Hu, Zhuo-Wei
影响因子：
15.9
作者：
Schaefer, L;Babelova, A;Gröne, HJ
通讯作者：
Gröne, HJ
DOI：
10.1084/jem.20070885
发表时间：
2007-11-26
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Nahrendorf M;Swirski FK;Aikawa E;Stangenberg L;Wurdinger T;Figueiredo JL;Libby P;Weissleder R;Pittet MJ
通讯作者：
Pittet MJ