Allcock R J, Peacock C D, Price P
Department of Microbiology, University of Western Australia, Nedlands, Australia.
J Leukoc Biol. 1996 Jul;60(1):44-50. doi: 10.1002/jlb.60.1.44.
We have shown that normal C57BL/6J mice are moderately resistant to infection with murine cytomegalovirus (MCMV) and that this resistance is impaired by prior infection with LP-BM5 MuLV, which causes a disease (MAIDS) similar to early HIV-induced disease. This study investigates macrophage function in MAIDS+ mice challenged with MCMV. MAIDS reduces the influx of cells into the peritoneal cavity seen in normal C57BL/6J mice 6 days after MCMV infection. The infiltrates contained cells that resembled activated macrophages, as they took up colloidal gold, expressed the macrophage marker Mac-1, had high levels of acid phosphatase activity, and were lymphocytostatic when co-cultured with activated T cells. MAIDS+ mice had a higher percentage of cells able to take up colloidal gold and higher acid phosphatase activity per cell. The cells were also more lymphocytostatic and produced higher levels of interleukin-1 and tumor necrosis factor-alpha on days 4 and 6 after MCMV infection. Hence, MAIDS enhances baseline and induced macrophage activity, but depresses infiltration into the site of inflammation.
我们已经表明,正常的C57BL/6J小鼠对鼠巨细胞病毒(MCMV)感染具有中度抵抗力,并且这种抵抗力会因先前感染LP-BM5 MuLV而受损,LP-BM5 MuLV会引发一种类似于早期HIV诱导疾病的病症(MAIDS)。本研究调查了受MCMV攻击的患MAIDS小鼠的巨噬细胞功能。MAIDS减少了正常C57BL/6J小鼠在MCMV感染6天后出现的细胞流入腹腔的情况。浸润细胞中含有类似于活化巨噬细胞的细胞,因为它们摄取胶体金,表达巨噬细胞标志物Mac-1,具有高水平的酸性磷酸酶活性,并且在与活化T细胞共培养时具有淋巴细胞抑制作用。患MAIDS小鼠中能够摄取胶体金的细胞百分比更高,且每个细胞的酸性磷酸酶活性更高。这些细胞在MCMV感染后的第4天和第6天也更具淋巴细胞抑制作用,并产生更高水平的白细胞介素-1和肿瘤坏死因子-α。因此,MAIDS增强了基线和诱导的巨噬细胞活性,但抑制了向炎症部位的浸润。