Tuning of the Hematopoietic Stem Cell Compartment in its Inflammatory Environment

Abstract

Purpose of review The hematopoietic stem cell (HSC) compartment is the cornerstone of a lifelong blood cell production but also contributes to the ability of the hematopoietic system to dynamically respond to environmental challenges. This review summarizes our knowledge about the interaction between HSCs and its inflammatory environment during life and questions how its disruption could affect the health of the hematopoietic system. Recent findings The latest research demonstrates the direct role of inflammatory signals in promoting the emergence of the HSCs during development and in setting their steady-state activity in adults. They indicate that inflammatory patho-physiological conditions or immunological history could shape the structure and biology of the HSC compartment, therefore altering its overall fitness. Summary Through instructive and/or selective mechanisms, the inflammatory environment seems to provide a key homeostatic signal for HSCs. Although the mechanistic basis of this complex interplay remains to be fully understood, its dysregulation has broad consequences on HSC physiology and the development of hematological diseases. As such, developing experimental models that fully recapitulate a normal basal inflammatory state could be essential to fully assess HSC biology in native conditions.

FOXO activity adaptation safeguards the hematopoietic stem cell compartment in hyperglycemia

“…These long-term conditions associated with hygiene, nutrition, or lifestyle directly affect the hematopoietic tissue and modulate the HSC native state. 4 Less acute but persistent over time, these conditions present a unique challenge to the maintenance of the long-lived HSCs. However, the mechanisms by which the HSC pool adapts to chronic stress conditions remain largely unknown.…”

Toll‐like receptors in the functional orientation of cardiac progenitor cells

“…Zhang, Rodriguez, et al, 2016). Some recent related studies demonstrated HSCs are assembled place for the low level of TLRs, however, their effects on HSCs has proved (Govindarajah & Reynaud, 2018). Takizawa et al (2017) confirmed that the mechanism of direct pathogen sensing in the replenishment of HSCs showed responsiveness of HSC inflammatory and proliferation responses, but it decreased their regenerative capacity against LPS via direct TLR4 stimulation.…”

“…Two important pathways have a key role in response to pathogenic and infectious agents, including TLRs and cytokine mechanism that leads to promote HSPCs (Takizawa et al, ). TLRs mechanism in HSPCs can recognize pathogenic agents directly by themselves (Govindarajah & Reynaud, ; H. Zhang, Rodriguez, et al, ). TLR4 is one of the TLR family expressed on hematopoietic cells activated by LPS ligand (Rosadini & Kagan, ).…”

“…Activation of NF‐kB and IRF‐3 can cause to produce transcription factors such as AP‐1 and IFN‐β signaling proteins, respectively that cause to enhancement in migration, differentiation, and proliferation, but the function of these pathways it is not completely clear (Liu et al, ; H. Zhang, Rodriguez, et al, ). Some recent related studies demonstrated HSCs are assembled place for the low level of TLRs, however, their effects on HSCs has proved (Govindarajah & Reynaud, ). Takizawa et al () confirmed that the mechanism of direct pathogen sensing in the replenishment of HSCs showed responsiveness of HSC inflammatory and proliferation responses, but it decreased their regenerative capacity against LPS via direct TLR4 stimulation.…”