The effect of the host's iron status on tuberculosis

被引：153

作者：

Boelaert, Johan R. ^{[1
]}

Vandecasteele, Stefaan J.

Appelberg, Rui

Gordeuk, Victor R.

机构：

[1] Acad Hosp St Jan, Unit Renal & Infect Dis, Ruddershovelaan 10, B-8000 Brugge, Belgium

[2] Univ Porto, Inst Mol & Cell Biol, P-4100 Oporto, Portugal

[3] Univ Porto, Inst Ciencias Biomed Abel Salazar, P-4100 Oporto, Portugal

[4] Howard Univ, Ctr Sickle Cell Dis, Washington, DC 20059 USA

来源：

JOURNAL OF INFECTIOUS DISEASES | 2007年 / 195卷 / 12期

关键词：

MYCOBACTERIUM-TUBERCULOSIS; HUMAN-MONOCYTES; IN-VITRO; ALVEOLAR MACROPHAGES; DECREASED RELEASE; INTERFERON-GAMMA; CHELATING-AGENTS; HIV-INFECTION; GROWTH; ACQUISITION;

D O I：

10.1086/518040

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Several lines of evidence have suggested that iron is critical for Mycobacterium tuberculosis growth in macrophages. Macrophage iron loading in patients with African iron overload increases the risk of tuberculosis (TB) and may worsen TB outcome. Likewise, macrophage iron loading may contribute to an increased predisposition toward TB in HIV infection. Human genetic disorders or variations may increase the risk of TB or worsen its outcome through macrophage iron loading, including the haptoglobin 2-2 phenotype, NRAMP1 polymorphisms (at least in Africans and Asians), and possibly ferroportin 1 mutations, but not HFE hemochromatosis. Thus, the host's iron status may be an important yet underevaluated factor in TB prevention and therapy and in TB vaccine design.

引用

页码：1745 / 1753

页数：9

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