Chandra R K, Au B, Woodford G, Hyam P
Ciba Found Symp. 1976(51):249-68. doi: 10.1002/9780470720325.ch12.
Nutritional factors can modulate immune responses. The concentration of iron, amongst other nutrients, influences host defence mechanisms. In experimentally induced iron deficiency in animals, morbidity and mortality on bacterial challenge are increased several-fold. Cell-mediated immunity and intra-cellular bacterial killing by polymorphonuclear leucocytes are impaired in iron-deficient individuals. This impairment is likely to be mediated by the effect of iron lack on cell proliferation, DNA synthesis and activity of iron-containing and iron-dependent enzymes involved in killing and elimination of microbes. Conversely, the availability of the free iron is a critical determinant for bacterial multiplication. It is not surprising then that epidemiological and clinical data on the frequency of infections--bacterial, fungal and others--in iron-deficient, iron-overloaded and healthy groups differ so widely. Vulnerability to infection based on the individual's iron status must be the net result of the effect of iron, or the lack of it, on microbial growth on the one hand and on immunocompetence of the host on the other. The key to keeping these interactions within physiological bounds is 'optimal iron nutrition'.
营养因素可调节免疫反应。铁的浓度与其他营养素一样，会影响宿主防御机制。在实验诱导的动物缺铁模型中，遭受细菌攻击时的发病率和死亡率会增加数倍。缺铁个体的细胞介导免疫以及多形核白细胞的细胞内细菌杀伤能力受损。这种损害可能是由缺铁对细胞增殖、DNA合成以及参与杀灭和清除微生物的含铁和铁依赖性酶活性的影响所介导的。相反，游离铁的可利用性是细菌繁殖的关键决定因素。因此，缺铁、铁过载和健康人群中细菌、真菌及其他感染频率的流行病学和临床数据差异如此之大也就不足为奇了。基于个体铁状态的感染易感性必然是铁或铁缺乏一方面对微生物生长、另一方面对宿主免疫能力影响的综合结果。将这些相互作用维持在生理范围内的关键是“最佳铁营养”。
