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锌缺乏与肠道/泌尿生殖道寄生虫相互作用导致安哥拉本哥省学龄前儿童贫血

Zinc Deficiency Interacts with Intestinal/Urogenital Parasites in the Pathway to Anemia in Preschool Children, Bengo-Angola.

机构信息

Centro de Investigação em Saúde de Angola (CISA), Caxito, Estação Central de Luanda, Apartado IV n °5547, Luanda 5547, Angola.

Departamento de Genética Humana, Avenida Padre Cruz, Instituto Nacional de Saúde Dr. Ricardo Jorge, 1649-016 Lisboa, Portugal.

出版信息

Nutrients. 2022 Mar 27;14(7):1392. doi: 10.3390/nu14071392.

Abstract

In host organisms with normal micronutrient status, nutritional immunity is a strongly regulated response aiming at decreasing the progression and severity of infections. Zinc deficiency may disturb this balance, impairing immune responses to infections, which may indirectly increase infection-related anemia. Since zinc deficiency may associate directly with anemia, the role of infections is often overlooked. Herein, we investigated the participation of infections (or inflammation) in the causal pathway between zinc deficiency and anemia. This transversal study, conducted in 2015 in Bengo-Angola, enrolled 852 under-3-year-old children. Logistic regression models were used to investigate interaction and mediation effects, and significance was confirmed by the Sobel test. In sum, 6.8% of children had zinc deficiency, 45.9% had anemia, and 15.6% had at least one intestinal/urogenital parasite. Furthermore, we found (1) no evidence that inflammation mediates or interacts with zinc deficiency to cause anemia, and (2) zinc deficiency interacts with infections, significantly increasing the odds of anemia (OR: 13.26, = 0.022). This interaction was stronger among children with iron deficiency anemia (OR: 46.66, = 0.003). Our results suggest that zinc deficiency may impair the immune response to infections and/or that intestinal parasites could have developed mechanisms to avoid zinc-limited environments. Further studies are needed to corroborate these suggestions.

摘要

在营养状况正常的宿主中,营养免疫是一种强烈调节的反应,旨在降低感染的进展和严重程度。锌缺乏可能会破坏这种平衡,损害对感染的免疫反应,这可能会间接增加与感染相关的贫血。由于锌缺乏可能直接与贫血有关,因此感染的作用往往被忽视。在此,我们研究了感染(或炎症)在锌缺乏和贫血之间因果关系中的作用。这项横断面研究于 2015 年在安哥拉本戈进行,共纳入了 852 名 3 岁以下儿童。使用逻辑回归模型来研究相互作用和中介效应,并通过 Sobel 检验确认显著性。结果显示,6.8%的儿童缺锌,45.9%的儿童贫血,15.6%的儿童至少有一种肠道/泌尿生殖道寄生虫。此外,我们发现(1)没有证据表明炎症在导致贫血的过程中起中介或相互作用;(2)锌缺乏与感染相互作用,显著增加了贫血的几率(OR:13.26, = 0.022)。这种相互作用在缺铁性贫血儿童中更为明显(OR:46.66, = 0.003)。我们的结果表明,锌缺乏可能会损害对感染的免疫反应,或者肠道寄生虫可能已经发展出了避免锌受限环境的机制。需要进一步的研究来证实这些假设。

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