Table 1.

Summary of inflammatory responses of HSC niche cells under different inflammatory/stress conditions.

Inflammation/Stress		Cell Type	Regulators	Inflammatory Responses	Reference
Chronic	Obesity	Adipocyte	TNF-α IL-1β IL-6	Adipocytes secreted diverse inflammatory cytokines and accumulated adipocytes impaired reconstitution potentials, increased myelopoiesis, and suppressed lymphopoiesis of HSCs	[77,79,80,81]
Chronic	MAPK-induced inflammation	Endothelial cell	NF-κB	Impaired HSC survival and functionality	[101]
Acute	pI:C/IFN-α administration	Endothelial cell	VEGF	Vasculature expansion by haematopoietic and non-haematopoietic pathways	[102]
Acute	Listeria monocytogenes infection	Endothelial cell	M-CSF	Loss of endothelial-derived CSF1 disrupted localisation of myeloid progenitors in perisinusoidal niche and, in turn, promoted dendritic cell generation	[103]
Acute	G-CSF administration	Macrophage (Osteomac)	n.d.	G-CSF administration depleted BM macrophages, and in turn, suppressed HSC-supportive osteoblasts	[104]
Acute	Haemolytic anaemia	Macrophage (Osteomac)	n.d.	The presence of macrophages is critical to erythroid recovery	[105]
Acute	Macrophage depletion	Macrophage (Osteomac)	n.d.	Macrophage depletion suppresses MSCs’ expression of HSC retention genes	[106]
Acute	5-FU	Megakaryocyte (MK)	FGF1	MKs supported HSC regeneration by increasing FG1 secretion	[107]
Chronic	Obesity	Megakaryocyte (MK)	IL-1β	Obesity augmented MK and platelet function and upregulated their inflammatory gene expressions	[108]
Chronic	Porphyromonas gingivalis infection	Megakaryocyte (MK)	IL-1β	Increased platelet production	[108]
Acute	TNF-α, IFN-γ, IL-1α/β signals	Mesenchymal stem cell (MSC)	IDO NO PGE2	Activated MSCs secreted immunosuppressive molecules inhibited T cell proliferation and activities	[28,109]
Acute	LCMV infection	Mesenchymal stem cell (MSC)	IFN-γ	LCMV infection disrupted structural morphology, network, and capability of HSC-supportive cytokine secretion of CAR cells	[110]
Acute	NP-CGG immunisation	Neutrophil	n.d.	Neutrophil emigration from BM to create a vacancy in BM to promote myeloid cell generation	[111]
Acute	Staphylococcus aureus infection	Osteoblast	G-CSF	Osteoblastic suppression by G-CSF impaired osteoblasts’ support to HSCs and promoted HSC mobilisation	[112,113,114]
Acute	Lithium treatment	Sympathetic nerve	β-catenin	Increased HSPC proliferation, mobilisation, and granulocyte colony formation	[115]
Acute	Adrenergic neurotransmitter treatment	Sympathetic nerve	β-catenin	Increased hCD34+ HSPC proliferation, mobilisation, and repopulating potential in vivo via canonical Wnt signalling pathway	[116]
Chronic	Neurotransmission ablation	Sympathetic nerve	G-CSF	Neurotransmission ablation suppressed HSC mobilisation and osteoblast function	[117,118]
Chronic	Altered circadian rhythms	Sympathetic nerve	CXCL12	Altered adrenergic signals disrupted rhythmic CXCL12 oscillations in BM and in turn dysregulation circadian HSC mobilisation	[119]
Acute	Allograft transplant	Treg cells	IL-10	The presence of Treg cells was critical to support the survival of allo-HSCs	[2]

n.d., not determined.