ArticlePloS one2018
Loss of murine Gfi1 causes neutropenia and induces osteoporosis depending on the pathogen load and systemic inflammation.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Genetic analysis of cis-enhancers associated with bone mineral density and periodontitis in the gene SOST.PloS one · 2025Article
- From inflammation to bone formation: the intricate role of neutrophils in skeletal muscle injury and traumatic heterotopic ossification.Experimental & molecular medicine · 2024Review
- The Inflammatory Contribution of B-Lymphocytes and Neutrophils in Progression to Osteoporosis.Cells · 2023Review
- Integrative profiling of gene expression and chromatin accessibility elucidates specific transcriptional networks in porcine neutrophils.Frontiers in genetics · 2023Article
- Neutrophil Elastase Defects in Congenital Neutropenia.Frontiers in immunology · 2021Review
- Immunoporosis: Role of Innate Immune Cells in Osteoporosis.Frontiers in immunology · 2021Review
- GFI-1 Protects Against Lipopolysaccharide-Induced Inflammatory Responses and Apoptosis by Inhibition of the NF-κB/TNF-α Pathway in H9c2 Cells.Inflammation · 2020Article
- Herpes zoster and the risks of osteoporosis and fracture: a nationwide cohort study.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2019Article
- Individual Effector/Regulator T Cell Ratios Impact Bone Regeneration.Frontiers in immunology · 2019Article
- Mouse Models and Tools for theFrontiers in immunology · 2019Review
- The Allergic Bone Marrow? The Immuno-Capacity of the Human Bone Marrow in Context of Metal-Associated Hypersensitivity Reactions.Frontiers in immunology · 2019Review
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gfi1 is a key molecule in hematopoietic lineage development and mutations in GFI1 cause severe congenital neutropenia (SCN). Neutropenia is associated with low bone mass, but the underlying mechanisms are poorly characterized. Using Gfi1 knock-out mice (Gfi1-ko/ko) as SCN model, we studied the relationship between neutropenia and bone mass upon different pathogen load conditions. Our analysis reveals that Gfi1-ko/ko mice kept under strict specific pathogen free (SPF) conditions demonstrate normal bone mass and survival. However, Gfi1-ko/ko mice with early (nonSPF) or late (SPF+nonSPF) pathogen exposure develop low bone mass. Gfi1-ko/ko mice demonstrate a striking rise of systemic inflammatory markers according to elevated pathogen exposure and reduced bone mass. Elevated inflammatory cytokines include for instance Il-1b, Il-6, and Tnf-alpha that regulate osteoclast development. We conclude that low bone mass, due to low neutrophil counts, is caused by the degree of systemic inflammation promoting osteoclastogenesis.
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