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      Inverse correlation between serum interleukin-6 and iron levels among Japanese adults: a cross-sectional study

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          Abstract

          Background

          Interleukin-6 (IL-6) is a multifunctional cytokine that is produced by many different cell types, and plays an important role in the regulation of inflammation, immune responses, the acute-phase response, and hematopoiesis. Previous laboratory and clinical studies have shown that IL-6 causes a significant decrease in serum iron levels. Therefore, we conducted an epidemiological study to examine the association between serum IL-6 and iron levels.

          Methods

          In total, 280 Japanese individuals aged 20–78 years were enrolled when they visited a clinic located in an urban area for Helicobacter pylori (H. pylori) infection tests and subsequent eradication; 65.3% were infected with H. pylori. Subjects with gastric cancer, idiopathic thrombocytopenia, or IL-6 > 10 pg/mL were excluded from the study. Serum iron and IL-6 levels were measured using the 2-nitroso-5-(N-propyl-3-sulfopropylamino) phenol method and chemiluminescence enzyme immunoassay, respectively.

          Results

          Geometric mean iron and IL-6 levels were 111.5 μg/dL and 1.77 pg/mL, respectively, for men, and 89.4 μg/dL and 1.55 pg/mL, respectively, for women. The logarithm of serum iron levels was negatively correlated with the logarithm of IL-6 levels in men (r = −0.19, p = 0.047), but not in women (r = −0.035, p = 0.65). Regression analysis, adjusted for sex, age, and H. pylori infection status, showed that the logarithm of serum iron levels was significantly associated with a decreased logarithm of IL-6 levels (β = −0.053, p = 0.041). The odds ratio for low serum iron levels adjusted for sex, age, and H. pylori infection status was 7.88 (95% CI 1.29–48.06) in those with an IL-6 level > 4 pg/mL.

          Conclusion

          Lower serum iron levels are significantly associated with higher serum IL-6 levels among Japanese adults.

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          Most cited references 27

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          IL-6 mediates hypoferremia of inflammation by inducing the synthesis of the iron regulatory hormone hepcidin.

          Hypoferremia is a common response to systemic infections or generalized inflammatory disorders. In mouse models, the development of hypoferremia during inflammation requires hepcidin, an iron regulatory peptide hormone produced in the liver, but the inflammatory signals that regulate hepcidin are largely unknown. Our studies in human liver cell cultures, mice, and human volunteers indicate that IL-6 is the necessary and sufficient cytokine for the induction of hepcidin during inflammation and that the IL-6-hepcidin axis is responsible for the hypoferremia of inflammation.
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            Hepcidin, a putative mediator of anemia of inflammation, is a type II acute-phase protein.

            Hepcidin is a liver-made peptide proposed to be a central regulator of intestinal iron absorption and iron recycling by macrophages. In animal models, hepcidin is induced by inflammation and iron loading, but its regulation in humans has not been studied. We report that urinary excretion of hepcidin was greatly increased in patients with iron overload, infections, or inflammatory diseases. Hepcidin excretion correlated well with serum ferritin levels, which are regulated by similar pathologic stimuli. In vitro iron loading of primary human hepatocytes, however, unexpectedly down-regulated hepcidin mRNA, suggesting that in vivo regulation of hepcidin expression by iron stores involves complex indirect effects. Hepcidin mRNA was dramatically induced by interleukin-6 (IL-6) in vitro, but not by IL-1 or tumor necrosis factor alpha (TNF-alpha), demonstrating that human hepcidin is a type II acute-phase reactant. The linkage of hepcidin induction to inflammation in humans supports its proposed role as a key mediator of anemia of inflammation.
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              Hepcidin and iron regulation, 10 years later.

               Tomas Ganz (2011)
              Under evolutionary pressure to counter the toxicity of iron and to maintain adequate iron supply for hemoglobin synthesis and essential metabolic functions, humans and other vertebrates have effective mechanisms to conserve iron and to regulate its concentration, storage, and distribution in tissues. The iron-regulatory hormone hepcidin, first described 10 years ago, and its receptor and iron channel ferroportin control the dietary absorption, storage, and tissue distribution of iron. Hepcidin causes ferroportin internalization and degradation, thereby decreasing iron transfer into blood plasma from the duodenum, from macrophages involved in recycling senescent erythrocytes, and from iron-storing hepatocytes. Hepcidin is feedback regulated by iron concentrations in plasma and the liver and by erythropoietic demand for iron. Genetic malfunctions affecting the hepcidin-ferroportin axis are a main cause of iron overload disorders but can also cause iron-restricted anemias. Modulation of hepcidin and ferroportin expression during infection and inflammation couples iron metabolism to host defense and decreases iron availability to invading pathogens. This response also restricts the iron supply to erythropoietic precursors and may cause or contribute to the anemia associated with infections and inflammatory disorders.
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                Author and article information

                Contributors
                Journal
                BMC Hematol
                BMC Hematol
                BMC Hematology
                BioMed Central
                2052-1839
                2014
                28 February 2014
                : 14
                : 6
                Affiliations
                [1 ]Department of Preventive Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan
                [2 ]Department of Hematology and Oncology, National Hospital Organization, Higashi Nagoya National Hospital, Nagoya, Japan
                [3 ]Department of Pathophysiological Laboratory Sciences, Nagoya University Graduate School of Medicine, Nagoya, Japan
                [4 ]Department of Healthcare Administration, Nagoya University Graduate School of Medicine, Nagoya, Japan
                Article
                2052-1839-14-6
                10.1186/2052-1839-14-6
                3974032
                24576354
                Copyright © 2014 Nakagawa et al.; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited.

                Categories
                Research Article

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