Diabetic pre-programming of myelopoiesis impairs tissue repair.

Bone marrow-derived monocyte-macrophages promote healing of injured tissue cooperatively with vasculogenic hematopoietic stem/progenitor cells. However, diabetes dysregulates hematopoiesis and attenuates bone marrow-derived tissue-reparative responses. In a recent issue of The Journal of Pathology, Barman et al extensively characterized myelopoietic responses in bone marrow following skin wounding in a type 2 model of diabetes. The study demonstrated that accumulation of monocyte-macrophages in the peripheral tissues is increased due to diabetic myelopoiesis that would oppose the reparative process following tissue injury. Interestingly, in this model, pathological myelopoiesis is independent of IL-1β. The potential prophylactic and therapeutic implications of these data are discussed in terms of paracrine signaling, macrophage polarization, and hematopoietic stem cell mobilization/retention.