关键词: Ancylostoma ceylanicum Anemia Hepcidin Hookworm infection Iron metabolism

Mesh : Humans Erythropoiesis / physiology Hepcidins / genetics Anemia / etiology Iron Erythropoietin / metabolism Hookworm Infections / complications

来  源:   DOI:10.1016/j.cyto.2024.156559

Abstract:
Over the years, there has been progress in understanding the molecular aspects of iron metabolism and erythropoiesis. However, despite research conducted both in laboratories and living organisms, there are still unanswered questions due to the complex nature of these fields. In this study we investigated the effects of hookworm infection on iron metabolism and how the hosts response to anemia is affected using hamsters infected with Ancylostoma ceylanicum as a model. Our data revealed interesting relationships between infection-induced anemia, erythropoiesis, iron metabolism, and immune modulation, such that the elevated production of erythropoietin (EPO) in renal tissue indicated intensified erythropoiesis in response to anemia. Additionally, the increased expression of the erythroferrone (ERFE) gene in the spleen suggested its involvement in iron regulation and erythropoiesis. Gene expression patterns of genes related to iron metabolism varied in different tissues, indicating tissue-specific adaptations to hypoxia. The modulation of pro-inflammatory and anti-inflammatory cytokines highlighted the delicate balance between immune response and erythropoiesis. Data derived from the investigation of changes induced in iron metabolism and stress erythropoiesis following anemia aid in our understanding of mechanisms related to blood spoliation and anemia, which could potentially be extrapolated or compared to other types or causes of anemia. These findings also contribute to our understanding of the pathophysiology of erythropoiesis in the context of blood loss.
摘要:
多年来,在了解铁代谢和红细胞生成的分子方面取得了进展。然而,尽管在实验室和生物体中都进行了研究,由于这些领域的复杂性,仍然存在悬而未决的问题。在这项研究中,我们研究了钩虫感染对铁代谢的影响,以及以感染Ancylostomaceylanicum的仓鼠为模型如何影响宿主对贫血的反应。我们的数据揭示了感染引起的贫血之间的有趣关系,红细胞生成,铁代谢,和免疫调节,因此,肾组织中促红细胞生成素(EPO)的产生增加表明贫血引起的红细胞生成增强。此外,脾脏中红细胞铁蛋白(ERFE)基因的表达增加表明其参与铁调节和红细胞生成。铁代谢相关基因的基因表达模式在不同组织中存在差异,表明对缺氧的组织特异性适应。促炎和抗炎细胞因子的调节突出了免疫应答和红细胞生成之间的微妙平衡。来自贫血后铁代谢和应激红细胞生成诱导变化的调查数据有助于我们理解与血液溶解和贫血相关的机制。这可能被推断或与其他类型的贫血或原因进行比较。这些发现也有助于我们对失血情况下红细胞生成的病理生理学的理解。
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