[Normal and emergency hematopoiesis: current concepts and clinical implications]

Recent advancements in techniques applied to the study of bone marrow histoarchitecture and the identification of genetic, epigenetic, proteomic, and metabolic characteristics of hematopoietic progenitor cells have facilitated a more comprehensive understanding of the interaction between these cells and the marrow microenvironment, as well as the mechanism of hematopoiesis. Hematopoiesis is maintained by primitive progenitor cells or stem cells, which undergo asymmetric division, enabling self-renewal. Pluripotent progenitor cells, which also possess self-renewal capabilities, are responsible for sustaining hematopoiesis. Hematopoietic progenitor cells represent a population in continuous and progressive differentiation towards mature cells, exhibiting plasticity to modify their proliferation and differentiation in response to received signals. In acute or chronic infections or inflammation, inflammatory cytokines and/or extracellular vesicles induce genetic, epigenetic, proteomic, and metabolic changes in hematopoietic progenitor cells, initiating emergency hematopoiesis. Emergency hematopoiesis constitutes an alteration of hematopoiesis characterized by: 1) increased myelopoiesis, with decreased lymphopoiesis and erythropoiesis, 2) increased release of hematopoietic progenitor cells into peripheral blood and development of extramedullary hemopoiesis, 3) generation of two cellular subpopulations of the innate immune system with defined characteristics and functions: a) innate immune memory cells (trained immunity), and b) myeloid suppressor cells. These changes can induce alterations in the neutrophil/lymphocyte and monocyte/lymphocyte ratio in the blood count, the increase of which has adverse prognostic value in various chronic inflammatory diseases and especially in neoplasms.