Do variations in mast cell hyperplasia account for differences in radiation-induced lung injury among different mouse strains, rats and nonhuman primates?
Do variations in mast cell hyperplasia account for differences in radiation-induced lung injury among different mouse strains, rats and nonhuman primates?
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DOI：
10.1667/rr3245.1
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发表时间：
2013-08
影响因子：
3.4
通讯作者：
Vujaskovic Z
中科院分区：
文献类型：
--
作者：
Down JD;Medhora M;Jackson IL;Cline JM;Vujaskovic Z
肥大细胞浸润在肺辐射损伤病理学中的作用是过去四十年来持续研究的主题。关于肥大细胞及其分泌产物如何参与急性炎症（肺炎）的产生和胶原沉积（纤维化）的慢性过程，已经提出了许多建议。另一个病理生理学检查肥大细胞增生和肺动脉高压之间可能的联系，通过释放血管活性介质。已知肺炎和纤维化的时间和程度在不同遗传小鼠品系和动物物种之间变化巨大。因此，我们系统地比较了肺切片中肥大细胞的数量从九个小鼠品系，两个大鼠品系和非人灵长类动物（NHP）后，全胸部照射（WTI）的剂量范围从10-15戈伊，并在进入呼吸窘迫的时间。BALB/c品系小鼠的间质肥大细胞数量显著增加，与WAG/Rij和August大鼠相似，而在其他小鼠品系（CBA、C3 H、B6、C57 L、WHT和TO小鼠）中观察到相对低水平的肥大细胞浸润。在10戈伊WTI后17周，5只NHP（恒河猴）表现出严重肺炎，肥大细胞计数也表明大多数小鼠品系的反应较低。肥大细胞反应与对肺炎或纤维化的菌株依赖性易感性之间似乎没有关系。需要进一步的调查，以探讨可能参与的肥大细胞在介导特定的血管反应，以及是否有遗传多样性的肥大细胞反应发生在人类。
The role of mast cell infiltrates in the pathology of radiation damage to the lung has been a subject of continuing investigation over the past four decades. This has been accompanied by a number of proposals as to how mast cells and the secretory products thereof participate in the generation of acute inflammation (pneumonitis) and the chronic process of collagen deposition (fibrosis). An additional pathophysiology examines the possible connection between mast cell hyperplasia and pulmonary hypertension through the release of vasoactive mediators. The timing and magnitude of pneumonitis and fibrosis are known to vary tremendously among different genetic mouse strains and animal species. Therefore, we have systematically compared mast cell numbers in lung sections from nine mouse strains, two rat strains and nonhuman primates (NHP) after whole thorax irradiation (WTI) at doses ranging from 10–15 Gy and at the time of entering respiratory distress. Mice of the BALB/c strain had a dramatic increase in interstitial mast cell numbers, similar to WAG/Rij and August rats, while relatively low levels of mast cell infiltrate were observed in other mouse strains (CBA, C3H, B6, C57L, WHT and TO mice). Enumeration of mast cell number in five NHPs (rhesus macaque), exhibiting severe pneumonitis at 17 weeks after 10 Gy WTI, also indicated a low response shared by the majority of mouse strains. There appeared to be no relationship between the mast cell response and the strain-dependent susceptibility towards pneumonitis or fibrosis. Further investigations are required to explore the possible participation of mast cells in mediating specific vascular responses and whether a genetically diverse mast cell response occurs in humans.