Dynamics of hematopoiesis is disrupted by impaired hematopoietic microenvironment in a mouse model of hemophagocytic lymphohistiocytosis.


Journal

Annals of hematology
ISSN: 1432-0584
Titre abrégé: Ann Hematol
Pays: Germany
ID NLM: 9107334

Informations de publication

Date de publication:
Jul 2020
Historique:
received: 11 02 2020
accepted: 17 05 2020
pubmed: 9 6 2020
medline: 24 7 2020
entrez: 8 6 2020
Statut: ppublish

Résumé

Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening systemic hyperinflammatory disorder. We found recently that repeated lipopolysaccharide (LPS) treatment induces HLH-like features in senescence-accelerated mice (SAMP1/TA-1) but not in senescence-resistant control mice (SAMR1). In this study, we analyzed the dynamics of hematopoiesis in this mouse model of HLH. When treated repeatedly with LPS, the numbers of myeloid progenitor cells (CFU-GM) and B-lymphoid progenitor cells (CFU-preB) in the bone marrow (BM) rapidly decreased after each treatment in both strains. The number of CFU-GM in SAMP1/TA-1 and SAMR1, and of CFU-preB in SAMR1, returned to pretreatment levels by 7 days after each treatment. However, the recovery in the number of CFU-preB in SAMP1/TA-1 was limited. In both strains, the BM expression of genes encoding positive regulators of myelopoiesis (granulocyte colony-stimulating factor (G-CSF), granulocyte macrophage colony-stimulating factor (GM-CSF), and interleukin (IL)-6), and negative regulators of B lymphopoiesis (tumor necrosis factor (TNF)-α) was increased. The expression of genes encoding positive regulators of B lymphopoiesis (stromal-cell derived factor (SDF)-1, IL-7, and stem cell factor (SCF)) was persistently decreased in SAMP1/TA-1 but not in SAMR1. Expression of the gene encoding p16

Identifiants

pubmed: 32506245
doi: 10.1007/s00277-020-04095-2
pii: 10.1007/s00277-020-04095-2
doi:

Substances chimiques

Lipopolysaccharides 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1515-1523

Subventions

Organisme : The Japan society for the promotion of science
ID : JP18K06846

Références

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Auteurs

Isao Tsuboi (I)

Division of Anatomical Science, Department of Functional Morphology, Nihon University School of Medicine, 30-1 Ohyaguchi-kami-machi, Itabashi-ku, Tokyo, 173-8610, Japan. tsuboi.isao@nihon-u.ac.jp.

Tomonori Harada (T)

Division of Anatomical Science, Department of Functional Morphology, Nihon University School of Medicine, 30-1 Ohyaguchi-kami-machi, Itabashi-ku, Tokyo, 173-8610, Japan.

Yoko Hirabayashi (Y)

Center for Biological Safety and Research, National Institute of Health Sciences, Kawasaki, Japan.

Shin Aizawa (S)

Division of Anatomical Science, Department of Functional Morphology, Nihon University School of Medicine, 30-1 Ohyaguchi-kami-machi, Itabashi-ku, Tokyo, 173-8610, Japan.

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