Macrophages can be divided on basis of their function: classically activated macrophages (M1) and alternatively activated macrophages (M2). Different endocrine stimuli influence macrophages differentiation. In this study, we verified the role of thyroid hormone (TH) system on macrophage differentiation/polarization through in vitro and in vivo approaches.

Primary cultures of differentiated macrophages (M[Fcy]) were obtained from mouse femur bone marrow derived cells. M[Fcy] were polarized to generate M1 and M2 subtypes. In these cells, we demonstrated different levels of TH receptors (TRa1, TRb1, and TRb2). Cells were then treated with TH during M[Fcy] differentiation, as well as during polarization to M1 or M2, and the TH-induced effects were determined. For instance, a set of specific cell-surface molecules and cytokine/receptor genes were measured. In addition, we determined TH effects on cell proliferation, cell viability, phagocytosis, arginase protein expression, cytokine release, and cell migration. In vivo experiments were also conducted in euthyroid/hypothyroid/hyperthyroid mice. In particular, we analysed the animal survival rate and the presence of cell-surface molecules in peritoneal macrophages of mice both in control conditions and during systemic inflammation. Our data suggest that TH has a role in modulating specific properties of macrophage populations and the functional balance M1/M2.