IRON LIMITATION AND THE GAMMA-INTERFERON-MEDIATED ANTIHISTOPLASMA STATE OF MURINE MACROPHAGES

被引：81

作者：

LANE, TE ^{[1
]}

WUHSIEH, BA ^{[1
]}

HOWARD, DH ^{[1
]}

机构：

[1] UNIV CALIF LOS ANGELES,SCH MED,DEPT MICROBIOL & IMMUNOL,LOS ANGELES,CA 90024

来源：

INFECTION AND IMMUNITY | 1991年 / 59卷 / 07期

关键词：

D O I：

10.1128/IAI.59.7.2274-2278.1991

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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.

引用

页码：2274 / 2278

页数：5

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