scholarly journals Infection and Reticuloendothelial System with special reference to iron metabolism

1963 ◽  
Vol 79 (1) ◽  
pp. 37-44 ◽  
Author(s):  
Mitsuto Hasegawa ◽  
Hiroshi Matsumoto
Keyword(s):  
Special Reference ◽  
Iron Metabolism ◽  
Reticuloendothelial System

scholarly journals A Short Review of Iron Metabolism and Pathophysiology of Iron Disorders

Medicines ◽  
2019 ◽  
Vol 6 (3) ◽  
pp. 85 ◽  
Author(s):  
Andronicos Yiannikourides ◽  
Gladys Latunde-Dada
Keyword(s):  
Iron Metabolism ◽  
Iron Homeostasis ◽  
Cellular Proliferation ◽  
Peptide Hormone ◽  
Short Review ◽  
Reticuloendothelial System ◽  
Cellular Level ◽  
Feedback Mechanism ◽  
The Body ◽  
Iron Regulatory Proteins

Iron is a vital trace element for humans, as it plays a crucial role in oxygen transport, oxidative metabolism, cellular proliferation, and many catalytic reactions. To be beneficial, the amount of iron in the human body needs to be maintained within the ideal range. Iron metabolism is one of the most complex processes involving many organs and tissues, the interaction of which is critical for iron homeostasis. No active mechanism for iron excretion exists. Therefore, the amount of iron absorbed by the intestine is tightly controlled to balance the daily losses. The bone marrow is the prime iron consumer in the body, being the site for erythropoiesis, while the reticuloendothelial system is responsible for iron recycling through erythrocyte phagocytosis. The liver has important synthetic, storing, and regulatory functions in iron homeostasis. Among the numerous proteins involved in iron metabolism, hepcidin is a liver-derived peptide hormone, which is the master regulator of iron metabolism. This hormone acts in many target tissues and regulates systemic iron levels through a negative feedback mechanism. Hepcidin synthesis is controlled by several factors such as iron levels, anaemia, infection, inflammation, and erythropoietic activity. In addition to systemic control, iron balance mechanisms also exist at the cellular level and include the interaction between iron-regulatory proteins and iron-responsive elements. Genetic and acquired diseases of the tissues involved in iron metabolism cause a dysregulation of the iron cycle. Consequently, iron deficiency or excess can result, both of which have detrimental effects on the organism.

Iron Metabolism in the Reticuloendothelial System

2003 ◽  
Vol 38 (1) ◽  
pp. 61-88 ◽  
Author(s):  
Mitchell Knutson ◽  
Marianne Wessling-Resnick
Keyword(s):  
Iron Metabolism ◽  
Reticuloendothelial System

scholarly journals Iron Reduces M1 Macrophage Polarization in RAW264.7 Macrophages Associated with Inhibition of STAT1

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Zhen-Shun Gan ◽  
Qian-Qian Wang ◽  
Jia-Hui Li ◽  
Xu-Liang Wang ◽  
Yi-Zhen Wang ◽  
...  
Keyword(s):  
Iron Metabolism ◽  
Iron Homeostasis ◽  
Macrophage Polarization ◽  
Reticuloendothelial System ◽  
Molecular Signature ◽  
Mrna Levels ◽  
M1 Macrophages ◽  
Iron Storage ◽  
Raw264.7 Macrophages ◽  
M1 Macrophage

Iron metabolism in inflammation has been mostly characterized in macrophages exposed to pathogens or inflammatory conditions. The aim of this study is to investigate the cross-regulatory interactions between M1 macrophage polarization and iron metabolism. Firstly, we characterized the transcription of genes related to iron homeostasis in M1 RAW264.7 macrophages stimulated by IFN-γ. The molecular signature of M1 macrophages showed high levels of iron storage (ferritin), a low level of iron export (ferroportin), and changes of iron regulators (hepcidin and transferrin receptors), which favour iron sequestration in the reticuloendothelial system and are benefit for inflammatory disorders. Then, we evaluated the effect of iron on M1 macrophage polarization. Iron significantly reduced mRNA levels of IL-6, IL-1β, TNF-α, and iNOS produced by IFN-γ-polarized M1 macrophages. Immunofluorescence analysis showed that iron also reduced iNOS production. However, iron did not compromise but enhanced the ability of M1-polarized macrophages to phagocytose FITC-dextran. Moreover, we demonstrated that STAT1 inhibition was required for reduction of iNOS and M1-related cytokines production by the present of iron. Together, these findings indicated that iron decreased polarization of M1 macrophages and inhibited the production of the proinflammatory cytokines. The results expanded our knowledge about the role of iron in macrophage polarization.

scholarly journals Is iron deficiency involved in the pathogenesis of chronic inflammatory skin disorders?

2019 ◽  
Vol 73 ◽  
pp. 359-363
Author(s):  
Małgorzata Ponikowska ◽  
Jacek C. Szepietowski
Keyword(s):  
Iron Deficiency ◽  
Iron Metabolism ◽  
Reticuloendothelial System ◽  
The Body ◽  
Iron Stores ◽  
Iron Supply ◽  
Tissue Iron ◽  
Bowel Disorders ◽  
Dermatological Disorders ◽  
Dermatologic Disease

Iron is an essential microelement in the human body due to its role in hematopoiesis, involvement in energetic processes, synthesis and decomposition of lipids, proteins and nuclear acids. Iron deficiency (ID) is common in healthy populations and also frequently coincides with natural course of chronic diseases. The former is typically present when the overall iron body storages are exhausted (absolute ID), most often due to insufficient iron supply, malabsorption or increased blood loss and coincides with anemia. The latter is a result of defected iron metabolism and reflects a condition, when despite adequate iron stores in the body, iron itself is trapped in the reticuloendothelial system, becoming unavailable for the metabolic processes. It typically occurs in the presence proinflammtory activation in chronic conditions such as chronic kidney disease, inflammatory bowel disorders, malignancies and heart failure. To date there are very few publications concerning the potential role of ID in chronic dermatological disorders. We have recently found that patients with psoriasis demonstrate pattern of ID which can be characterized by negative tissue iron balance with depleted iron stores in the body. Interestingly, presence of ID was not related to the severity of psoriasis, but rather determined by patients low body mass index. We are currently investigating the hypothesis that derangements in iron metabolism resulting in ID can be also present in hidradenitis suppurativa – the other chronic dermatologic disease associated with inflammatory and autoimmune activation.

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