铁限制与γ干扰素介导的小鼠巨噬细胞抗组织胞浆菌状态
Iron limitation and the gamma interferon-mediated antihistoplasma state of murine macrophages.
作者信息
Lane T E, Wu-Hsieh B A, Howard D H
机构信息
Department of Microbiology and Immunology, University of California School of Medicine, Los Angeles 90024.
出版信息
Infect Immun. 1991 Jul;59(7):2274-8. doi: 10.1128/iai.59.7.2274-2278.1991.
Abstract
The zoopathogenic fungus Histoplasma capsulatum requires iron for growth. Intracellular growth of the fungus within mouse peritoneal macrophages is inhibited by recombinant murine gamma interferon (IFN-gamma). Such treatment of mouse peritoneal macrophages induces a marked downshift in transferrin receptors. We tested whether the antihistoplasma effect of IFN-gamma-treated macrophages is the result of iron deprivation. Treatment of mouse peritoneal macrophages with the intracellular iron chelator deferoxamine inhibits the intracellular growth of H. capsulatum. Exposure of macrophages to holotransferrin antagonizes the effect of both recombinant murine IFN-gamma and deferoxamine treatments. These results suggest that iron restriction may be one of the bases for the IFN-gamma-induced antihistoplasma effect of mouse macrophages.
摘要
动物致病性真菌荚膜组织胞浆菌生长需要铁。重组小鼠γ干扰素（IFN-γ）可抑制该真菌在小鼠腹腔巨噬细胞内的生长。对小鼠腹腔巨噬细胞进行此类处理会导致转铁蛋白受体显著下调。我们测试了经IFN-γ处理的巨噬细胞的抗组织胞浆菌作用是否是铁缺乏的结果。用细胞内铁螯合剂去铁胺处理小鼠腹腔巨噬细胞可抑制荚膜组织胞浆菌的细胞内生长。巨噬细胞暴露于全转铁蛋白可拮抗重组小鼠IFN-γ和去铁胺处理的效果。这些结果表明，铁限制可能是IFN-γ诱导小鼠巨噬细胞产生抗组织胞浆菌作用的基础之一。
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