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首页> 外文期刊>Journal of dermatological science >TLR4, rather than TLR2, regulates wound healing through TGF-β and CCL5 expression
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TLR4, rather than TLR2, regulates wound healing through TGF-β and CCL5 expression

机译：TLR4而非TLR2通过TGF-β和CCL5表达调节伤口愈合

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Background: Toll-like receptors (TLRs) have a crucial role in early host defense against invading pathogens. Recent studies suggest that TLRs play important roles in non-infections inflammation and tissue repair and regeneration. Objective: To determine the roles of TLR2 and TLR4 in mouse wound healing using TLR2-deficient (TLR2-/-), TLR4-deficient (TLR4-/-), and TLR2/TLR4-deficient (TLR2/4-/-) mice. Methods: Open wounds made in TLR2-/-, TLR4-/-, and TLR2/4-/- mice were examined clinically and histologically. Cytokine expression in the wounded skin was also investigated. TGF-β production from macrophages stimulated by hyaluronan, a ligand for TLR2 and TLR4, was evaluated by real-time PCR. Results: Wound areas in TLR2-/-, TLR4-/-, and TLR2/4-/- mice were larger than wild-type mice both at days 3 and 7 after wounding, accompanied by decreased numbers of infiltrating macrophages in the dermis and decreased TGF-β and CCL5 mRNA expression in the wounded skin. Immunohistochemistry showed decreased numbers of macrophages expressing TGF-β and reduced CCL5 expression by keratinocytes in the wounded skin from TLR2-/-, TLR4-/-, and TLR2/4-/- mice compared to wild-type mice. Moreover, TGF-β production from macrophages induced by hyaluronan stimulation in vitro was significantly decreased in the absence of TLRs, especially TLR4. Interestingly, macrophages and wounded skin from TLR2-/- mice showed decreased TLR4 mRNA expression compared to wild-type mice, suggesting that the effect of TLR2 deficiency was at least partially dependent on decrease in TLR4. Topical application of TGF-β and CCL5 significantly improved wound healing in TLR-deficient mice. Conclusion: TLR4, rather than TLR2, regulates wound healing through TGF-β and CCL5 expression.
机译：背景：Toll样受体（TLR）在早期宿主防御入侵病原体中起着至关重要的作用。最近的研究表明，TLR在非感染性炎症以及组织修复和再生中起重要作用。目的：确定TLR2和TLR4在TLR2缺陷（TLR2-/-），TLR4缺陷（TLR4-/-）和TLR2 / TLR4缺陷（TLR2 / 4-/-）小鼠伤口愈合中的作用。方法：临床和组织学检查TLR2-/-，TLR4-/-和TLR2 / 4-/-小鼠的开放性伤口。还研究了受伤皮肤中细胞因子的表达。通过实时PCR评估了由透明质酸刺激的巨噬细胞产生的TGF-β，透明质酸是TLR2和TLR4的配体。结果：受伤后第3天和第7天，TLR2-/-，TLR4-/-和TLR2 / 4-/-小鼠的伤口面积均比野生型小鼠大，同时真皮和肝脏中的巨噬细胞浸润数量减少。降低了受伤皮肤中TGF-β和CCL5 mRNA的表达。免疫组织化学显示，与野生型小鼠相比，TLR2-/-，TLR4-/-和TLR2 / 4-/-小鼠受伤皮肤中表达TGF-β的巨噬细胞数量减少，角质形成细胞CCL5表达减少。而且，在不存在TLR，尤其是TLR4的情况下，透明质酸刺激体外诱导的巨噬细胞产生的TGF-β明显降低。有趣的是，与野生型小鼠相比，TLR2-/-小鼠的巨噬细胞和受伤的皮肤显示TLR4 mRNA表达降低，这表明TLR2缺乏症的影响至少部分取决于TLR4的降低。 TGF-β和CCL5的局部应用可显着改善TLR缺陷小鼠的伤口愈合。结论：TLR4而非TLR2通过TGF-β和CCL5表达调节伤口愈合。

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