PDF(Pubmed)
Abstract：
Thousands struggle with acute and chronic intestinal injury due to various causes. Epithelial intestinal healing is dependent on phenotypic transitions to a mobile phenotype. Focal adhesion kinase (FAK) is a ubiquitous protein that is essential for cell mobility. This phenotype change is mediated by FAK activation and proves to be a promising target for pharmaceutical intervention. While FAK is crucial for intestinal healing, new evidence connects FAK with innate immunity and the importance it plays in macrophage/monocyte chemotaxis, as well as other intracellular signaling cascades. These cascades play a part in macrophage/monocyte polarization, maturation, and inflammation that is associated with intestinal injury. Colony stimulating factors (CSFs) such as macrophage colony stimulating factor (M-CSF/CSF-1) and granulocyte macrophage colony stimulating factor (GM-CSF/CSF-2) play a critical role in maintaining homeostasis within intestinal mucosa by crosstalk capabilities between macrophages and epithelial cells. The communication between these cells is imperative in orchestrating healing upon injury. Diving deeper into these connections may allow us a greater insight into the role that our immune system plays in healing, as well as a better comprehension of inflammatory diseases of the gut.
摘要：
由于各种原因，成千上万的人与急性和慢性肠道损伤作斗争。肠上皮愈合依赖于表型向移动表型的转变。粘着斑激酶（FAK）是一种普遍存在的蛋白质，对细胞的移动性至关重要。这种表型变化是由FAK激活介导的，并被证明是药物干预的有希望的目标。虽然FAK对肠道愈合至关重要，新的证据将FAK与先天免疫以及它在巨噬细胞/单核细胞趋化中的重要性联系起来，以及其他细胞内信号级联。这些级联在巨噬细胞/单核细胞极化中起作用，成熟,以及与肠道损伤相关的炎症。集落刺激因子(CSF)如巨噬细胞集落刺激因子(M-CSF/CSF-1)和粒细胞巨噬细胞集落刺激因子(GM-CSF/CSF-2)通过巨噬细胞和上皮细胞之间的串扰能力在维持肠粘膜内的稳态中起关键作用。这些细胞之间的交流对于协调受伤后的愈合至关重要。深入研究这些联系可能会让我们更深入地了解我们的免疫系统在康复中的作用，以及对肠道炎症性疾病的更好理解。
