In response to inflammatory stimuli (eg, infection and injury) hematopoietic stem and progenitor cells (HSPCs) proliferate and differentiate, giving rise to the effector cell types necessary to fight the acute insult. While this is an important part of the normal immune response, sustained or aberrant exposure to inflammatory signals can lead to a loss of HSPC function. Accumulating reports demonstrate that inflammatory cytokines (eg, IFNγ, IFNα/β, and TNFα), and even pathogens or cell damage-associated ligands, can influence the function of HSPCs via both direct and indirect mechanisms and may contribute to clinically significant disorders of HSPCs including bone marrow (BM) failure and hematopoietic malignancies.

In this topic, we explore the effects of infections and their associated inflammatory cytokines on HSPCs. The seven reviews and one original article within this topic cover the role of inflammatory signals in regulating HSPCs from their ontogeny through old age and discuss the contribution of these signals to BM dysfunction and leukemogenesis. Furthermore, they highlight the unique effects of different pathogens and cytokines on HSPCs and discuss the direct, cell-autonomous effects of inflammation on HSPCs versus the indirect effects that are mediated by alterations in stromal cells and other cells within the BM microenvironment.