Effects of iron deficiency on the activation of glial cells against an antigenic challenge

Abstract

Iron is an essential element for the central nervous system (CNS). Microglia and astrocytes are involved in CNS immunity. The aim of this study was to determine the effect of iron deficiency on the activation capacity of microglia and astrocytes challenged with bacterial lipopolysaccharide (LPS). We studied the activation of signaling cascades involving the transcription factors NF‐KB, AP‐1 and STAT 1 and 3, which promote the production of proinflammatory cytokines. Glial cells from newborn BALB/c mice were cultured 15 days. 24 hrs before LPS challenge, cells were treated with the iron quelator deferoxamine. Western blot (WB) analysis showed PKC phosphorylation as soon as 30 min after LPS stimulation in iron deficient cells (dFe). PKC protein phosphorylation was altered compared with control cells (sFe). JNK and ERK phosphorylation disappeared 30 minutes post‐stimulation in sFe cells, whereas phosphorylation was sustained up to 1 hr in dFe cells. Finally, we determined that dFe cells produced more NO than sFe after LPS stimulation. We are currently studying the nuclear translocation of NF‐KB and STAT to corroborate if iron deficiency alters the signaling cascades involving these molecules. Altogether, our data suggests that iron deficiency leads to an increased activation of glial cells after antigenic challenge.