Effects of IL-10 on iron metabolism in LPS-induced inflammatory mice via modulating hepcidin expression

Body's iron metabolism is at one dynamic balance status, and abnormal iron metabolism may lead to renal anemia. Inflammation stimuli may lead to abnormal iron metabolism and aggravation of chronic failure anemia. Hepcidin can regulate iron metabolic homeostasis, further mediating renal anemia. Interleukin-10 (IL-10) is an inflammatory inhibitor, but with an unclear function in the regulation of hepcidin expression.

BALB/c mice were randomly assigned into three groups: control group; lipid polysaccharide (LPS) group, which received 0.1 mg/kg LPS via tail veins; IL-10 group with 0.2 mg/kg IL-10 injection after LPS. Red blood cell count (RBC), hemoglobulin (Hb), hematocrit (HCT), mean corpuscular volume (MCV) and iron content in hemoglobulin were measured. Real-time PCR quantified hepcidin mRNA expression in all groups. Enzyme linked immunosorbent assay (ELISA) tested serum hepcidin, IL-6 and tumor necrosis factor-α (TNF-α) levels. Western blot analyzed expression of mouse transferrin receptor 2 (TfR2) and hepcidin signal pathway molecule STAT3.

LPS model group had lower RBC, Hb, HCT, MCV and iron content in Hb, plus elevated hepcidin, IL-6, TNF-α, TfR2 and STAT3 expression (p < 0.05 compared to the control group). IL-10 treatment group significantly facilitated RBC, Hb, HCT, MCV and Hb iron contents in LPS-induced inflammatory model mice, which also had lower hepcidin, IL-6, TNF-α, TfR2 or STAT3 expression (p < 0.05 compared to LPS group).

IL-10 can improve iron metabolism and alleviate anemia via suppressing inflammatory factor, modulating STAT3 signal pathway, down-regulating hepcidin expression and inhibiting TfR expression.