Innate Immune System Activation, Inflammation and Corneal Wound Healing.
Innate Immune System Activation, Inflammation and Corneal Wound Healing.
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DOI：
10.3390/ijms232314933
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发表时间：
2022-11-29
影响因子：
5.6
通讯作者：
中科院分区：
文献类型：
--
作者：
由损伤、手术或其他侵入引起的角膜伤口不仅引起疼痛，而且还可能使个体易于感染。虽然一些炎症可能有益于防止伤口的微生物感染，但如果过度，则炎症过程可能会延迟角膜伤口愈合。关于炎症对角膜伤口愈合影响的文献检查表明，导致严重或慢性炎症减少的操作在角膜透明度、厚度和愈合方面产生更好的结果。然而，一些急性炎症是必要的，以允许有效的细菌和真菌清除，并防止角膜感染。这种炎症可以由微生物成分触发，这些微生物成分通过Toll样受体（TLR）途径激活先天免疫系统。特别是，TLR 2和TLR 4活化导致活化B细胞（NFκB）的促炎性核因子κ轻链增强子活化。类似地，从破坏的细胞释放的内源性分子（称为损伤相关分子模式（DAMP））也可以激活TLR 2、TLR 4和NFκB，由此产生的炎症使角膜伤口愈合的结果恶化。在无感染的无菌性角膜炎中，炎症可通过TLR发生，从而影响角膜伤口愈合并降低角膜透明度。这篇综述表明，需要急性炎症，以防止病原体浸润，同时支持的想法，减少慢性和/或过度炎症将允许改善伤口愈合。
Corneal wounds resulting from injury, surgeries, or other intrusions not only cause pain, but also can predispose an individual to infection. While some inflammation may be beneficial to protect against microbial infection of wounds, the inflammatory process, if excessive, may delay corneal wound healing. An examination of the literature on the effect of inflammation on corneal wound healing suggests that manipulations that result in reductions in severe or chronic inflammation lead to better outcomes in terms of corneal clarity, thickness, and healing. However, some acute inflammation is necessary to allow efficient bacterial and fungal clearance and prevent corneal infection. This inflammation can be triggered by microbial components that activate the innate immune system through toll-like receptor (TLR) pathways. In particular, TLR2 and TLR4 activation leads to pro-inflammatory nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) activation. Similarly, endogenous molecules released from disrupted cells, known as damage-associated molecular patterns (DAMPs), can also activate TLR2, TLR4 and NFκB, with the resultant inflammation worsening the outcome of corneal wound healing. In sterile keratitis without infection, inflammation can occur though TLRs to impact corneal wound healing and reduce corneal transparency. This review demonstrates the need for acute inflammation to prevent pathogenic infiltration, while supporting the idea that a reduction in chronic and/or excessive inflammation will allow for improved wound healing.
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影响因子：
3.7
作者：
Huang W;Ling S;Jia X;Lin B;Huang X;Zhong J;Li W;Lin X;Sun Y;Yuan J
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影响因子：
4.1
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通讯作者：
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影响因子：
3.3
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影响因子：
2.6
作者：
Babizhayev, Mark A.;Strokov, Igor A.;Lankin, Vadim Z.
通讯作者：
Lankin, Vadim Z.
影响因子：
4.4
作者：
Bollag, Wendy B.;Olala, Lawrence O.;Watsky, Mitchell
通讯作者：
Watsky, Mitchell