Fig. 2.
Effect of parenteral iron administration on inflammatory gene expression and serum cytokine levels. Serum, lung, and liver samples were harvested from C57Bl/6 mice treated with iron and/or lipopolysaccharide (LPS) and analyzed for serum Il6 (A), serum Tnfα (B), and mRNA levels of the two cytokines in the lungs (C, D) and livers (E, F). In each case, iron supplementation by itself did not induce inflammation. Lipopolysaccharide alone induced increases in cytokine protein levels, as well as mRNA levels. Serum cytokine levels in the control and iron-treated groups were below the detection level of the assay in many cases. Iron administration significantly enhanced the effect of lipopolysaccharide-induced inflammation in the mice. N = 7 to 9 mice per group (Mann–Whitney U test [A, B] and two-way ANOVA with Bonferroni post hoc tests [C–F]; P values adjusted for all possible comparisons). Il = interleukin; Int = interaction P value; TNF, tumor necrosis factor.

Effect of parenteral iron administration on inflammatory gene expression and serum cytokine levels. Serum, lung, and liver samples were harvested from C57Bl/6 mice treated with iron and/or lipopolysaccharide (LPS) and analyzed for serum Il6 (A), serum Tnfα (B), and mRNA levels of the two cytokines in the lungs (C, D) and livers (E, F). In each case, iron supplementation by itself did not induce inflammation. Lipopolysaccharide alone induced increases in cytokine protein levels, as well as mRNA levels. Serum cytokine levels in the control and iron-treated groups were below the detection level of the assay in many cases. Iron administration significantly enhanced the effect of lipopolysaccharide-induced inflammation in the mice. N = 7 to 9 mice per group (Mann–Whitney U test [A, B] and two-way ANOVA with Bonferroni post hoc tests [C–F]; P values adjusted for all possible comparisons). Il = interleukin; Int = interaction P value; TNF, tumor necrosis factor.

Close Modal

or Create an Account

Close Modal
Close Modal