Hayashi K, Kurata T, Morishima T, Nassery T
Infect Immun. 1980 May;28(2):350-8. doi: 10.1128/iai.28.2.350-358.1980.
Peritoneal macrophages obtained from mice after an intraperitoneal injection of tryptose peptone inhibited the development of herpes simplex virus type 2 plaques in syngeneic mouse embryonic fibroblasts. In contrast, peritoneal macrophages, spleen cells, and thymocytes from untreated mice showed only a minimal inhibitory effect on the development of viral plaques. The effect was age dependent. Macrophages from 2 and 3-week-old mice showed weaker functions, requiring a larger number of cells for an equivalent reduction of plaques and virus yield than those from adult mice. When macrophages were treated with procaine, their phagocytic activity was completely abolished. However the procaine-treated macrophages still could inhibit the development of viral plaques. Peritoneal macrophages did not show any increased cytotoxicity against herpes simplex virus-infected cells; plaque inhibition might rather be attributable to their cytostatic effects on target cells.
腹腔注射胰蛋白胨后从小鼠获得的腹腔巨噬细胞抑制了同基因小鼠胚胎成纤维细胞中单纯疱疹病毒2型蚀斑的形成。相比之下,未处理小鼠的腹腔巨噬细胞、脾细胞和胸腺细胞对病毒蚀斑的形成仅表现出最小程度的抑制作用。该作用具有年龄依赖性。2周龄和3周龄小鼠的巨噬细胞功能较弱,与成年小鼠相比,需要更多数量的细胞才能同等程度地减少蚀斑和病毒产量。当巨噬细胞用普鲁卡因处理时,其吞噬活性完全丧失。然而,经普鲁卡因处理的巨噬细胞仍然能够抑制病毒蚀斑的形成。腹腔巨噬细胞对单纯疱疹病毒感染的细胞未表现出任何增加的细胞毒性;蚀斑抑制可能更多归因于它们对靶细胞的细胞生长抑制作用。