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首页> 外文期刊>Biomaterials >Critical role of tissue mast cells in controlling long-term glucose sensor function in vivo.
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Critical role of tissue mast cells in controlling long-term glucose sensor function in vivo.

机译：组织肥大细胞在控制体内长期葡萄糖传感器功能中的关键作用。

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Little is known about the specific cells, mediators and mechanisms involved in the loss of glucose sensor function (GSF) in vivo. Since mast cells (MC) are known to be key effector cells in inflammation and wound healing, we hypothesized that MC and their products are major contributors to the skin inflammation and wound healing that controls GSF at sites of sensor implantation. To test this hypothesis we utilized a murine model of continuous glucose monitoring (CGM) in vivo in both normal C57BL/6 mice (mast cell sufficient), as well as mast cell deficient B6.Cg-Kit(W-sh)/HNihrJaeBsmJ (Sash) mice over a 28 day CGM period. As expected, both strains of mice displayed excellent CGM for the first 7 days post sensor implantation (PSI). CGM in the mast cell sufficient C57BL/6 mice was erratic over the remaining 21 days PSI. CGM in the mast cell deficient Sash mice displayed excellent sensor function for the entire 28 day of CGM. Histopathologic evaluation of implantation sites demonstrated that tissue reactions in Sash mice were dramatically less compared to the reactions in normal C57BL/6 mice. Additionally, mast cells were also seen to be consistently associated with the margins of sensor tissue reactions in normal C57BL/6 mice. Finally, direct injection of bone marrow derived mast cells at sites of sensor implantation induced an acute and dramatic loss of sensor function in both C57BL/6 and Sash mice. These results demonstrate the key role of mast cells in controlling glucose sensor function in vivo.
机译：对于体内葡萄糖传感器功能丧失（GSF）涉及的特定细胞，介体和机制知之甚少。由于已知肥大细胞（MC）是炎症和伤口愈合中的关键效应细胞，因此我们假设MC及其产品是控制传感器植入部位GSF的皮肤炎症和伤口愈合的主要因素。为了验证这一假设，我们在正常C57BL / 6小鼠（肥大细胞充足）以及肥大细胞缺乏B6.Cg-Kit（W-sh）/ HNihrJaeBsmJ（腰带）小鼠在28天的CGM期间内。如预期的那样，两种小鼠品系在传感器植入（PSI）后的前7天均表现出出色的CGM。在剩余的21天PSI中，肥大细胞中的CGM足够，C57BL / 6小鼠不稳定。肥大细胞缺乏的Sash小鼠中的CGM在CGM的整个28天中表现出出色的传感器功能。植入部位的组织病理学评估表明，与正常C57BL / 6小鼠相比，Sash小鼠的组织反应明显减少。此外，在正常的C57BL / 6小鼠中，肥大细胞也被认为与传感器组织反应的边缘一致。最后，在传感器植入部位直接注射骨髓衍生的肥大细胞在C57BL / 6和Sash小鼠中均导致了传感器功能的急性和戏剧性丧失。这些结果证明了肥大细胞在体内控制葡萄糖传感器功能中的关键作用。

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