Abstract
Iodine is an essential element required for the function of all organ systems. Although the importance of iodine in thyroid hormone synthesis and reproduction is well known, its direct effects on the immune system are elusive. Human leukocytes expressed mRNA of iodide transporters (NIS and PENDRIN) and thyroid-related proteins [thyroglobulin (TG) and thyroid peroxidase (TPO)]. The mRNA levels of PENDRIN and TPO were increased whereas TG transcripts were decreased post leukocyte activation. Flow cytometric analysis revealed that both PENDRIN and NIS were expressed on the surface of leukocyte subsets with the highest expression occurring on monocytes and granulocytes. Treatment of leukocytes with sodium iodide (NaI) resulted in significant changes in immunity-related transcriptome with an emphasis on increased chemokine expression as probed with targeted RNASeq. Similarly, treatment of leukocytes with NaI or Lugol’s iodine induced increased protein production of both pro- and anti-inflammatory cytokines. These alterations were not attributed to iodide-induced de novo thyroid hormone synthesis. However, upon incubation with thyroid-derived TG, primary human leukocytes but not Jurkat T cells released thyroxine and triiodothyronine indicating that immune cells could potentially influence thyroid hormone balance. Overall, our studies reveal the novel network between human immune cells and thyroid-related molecules and highlight the importance of iodine in regulating the function of human immune cells.
Highlights
Iodine is an essential mineral required for the biosynthesis of thyroid hormones and subsequent proper function of metabolic pathways of all body organs [1]
Activation of leukocytes with PMA and ionomycin (PMA-IO) induced a substantial increase of mRNA levels of PENDRIN but not NIS (Figure 1A). qPCR with TaqMan probes confirmed no significant change in NIS expression, but approximately eightfold increase of PENDRIN mRNA upon activation of leukocytes (Figure 1B)
Analysis of iodide receptor expression on leukocyte subsets demonstrated that phagocytes, monocytes, and granulocytes harbor the highest expression of iodide transporters (Figures 1C,D)
Summary
Iodine is an essential mineral required for the biosynthesis of thyroid hormones and subsequent proper function of metabolic pathways of all body organs [1]. The requirement for sufficient iodine levels encompasses all stages of life [2, 4]. Increased iodine levels are required during pregnancy, and reduced amounts lead to miscarriages and reproductive failures [5,6,7,8]. This is in-part due to the role of iodine-derived thyroid hormones, thyroxine (T4), and triiodothyronine (T3), for optimal fetal brain development [9, 10]. Congenital hypothyroidism, defined by reduced thyroid hormones leading to stunted mental and physical development during early childhood, is caused by insufficient iodine
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