ArticleNature communications2018
Bone marrow lympho-myeloid malfunction in obesity requires precursor cell-autonomous TLR4.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
36 citing papers in PubMed, 53 citations in OpenAlex.
- Alcohol consumption exacerbates high-fat diet-mediated disruptions in myelopoiesis and osteoclastogenesis in mouse models of metabolic dysfunction-associated liver diseases.Frontiers in endocrinology · 2026Article
- Diet-induced obesity induces oxidative stress and enhances H3K4me3 levels, driving nonresolving inflammation and myelopoiesis in hematopoietic stem and progenitor cells.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Bone Marrow Niche in Cardiometabolic Disease: Mechanisms and Therapeutic Potential.Circulation research · 2025Review
- Obesity modulates hematopoietic stem cell fate decision via IL-1β induced p38/MAPK signaling pathway.Stem cell research & therapy · 2024Article
- Bone marrow inflammatory memory in cardiometabolic disease and inflammatory comorbidities.Cardiovascular research · 2024Review
- The parasitic worm product ES-62 protects against collagen-induced arthritis by resetting the gut-bone marrow axis in a microbiome-dependent manner.Frontiers in tropical diseases · 2024Article
- Maternal vitamin B1 is a determinant for the fate of primordial follicle formation in offspring.Nature communications · 2023Article
- Bone Marrow Adipose Tissue: Regulation of Osteoblastic Niche, Hematopoiesis and Hematological Malignancies.Stem cell reviews and reports · 2023Review
- Macrophage function in adipose tissue homeostasis and metabolic inflammation.Nature immunology · 2023Review
- Bioinformatics and system biology approach to identify the influences of SARS-CoV-2 on metabolic unhealthy obese patients.Frontiers in molecular biosciences · 2023Article
- Maternal Western-style diet remodels the transcriptional landscape of fetal hematopoietic stem and progenitor cells in rhesus macaques.Stem cell reports · 2022Article
- How Does Lifestyle Affect Hematopoiesis and the Bone Marrow Microenvironment?Toxicologic pathology · 2022Review
- Relationship Between BMI and Disease Severity in COVID-19 Patients.Anesthesiology and pain medicine · 2022Article
- Obesity, Bone Loss, and Periodontitis: The Interlink.Biomolecules · 2022Review
- Modulation of Gut Microbiota Metabolism in Obesity-Related Type 2 Diabetes Reduces Osteomyelitis Severity.Microbiology spectrum · 2022Article
- Hematopoietic Progenitors and the Bone Marrow Niche Shape the Inflammatory Response and Contribute to Chronic Disease.International journal of molecular sciences · 2022Review
- The Role of Nutrients in Maintaining Hematopoietic Stem Cells and Healthy Hematopoiesis for Life.International journal of molecular sciences · 2022Review
- The parasitic worm product ES-62 protects the osteoimmunology axis in a mouse model of obesity-accelerated ageing.Frontiers in immunology · 2022Article
- The Traditional Mongolian Medicine Qiqirigan-8 Effects on Lipid Metabolism and Inflammation in Obesity: Pharmacodynamic Evaluation and Relevant Metabolites.Frontiers in pharmacology · 2022Article
- You are what you eat: How to best fuel your immune system.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Obesity, a prevalent condition in adults and children, impairs bone marrow (BM) function. However, the underlying mechanisms are unclear. Here, we show that obese mice exhibit poor emergency immune responses in a toll-like receptor 4 (TLR4)-dependent manner. Canonical myeloid genes (Csf1r, Spi1, Runx1) are enhanced, and lymphoid genes (Flt3, Tcf3, Ebf1) are reduced. Using adoptive transfer and mixed BM chimera approaches we demonstrate that myeloid>lymphoid bias arises after 6 weeks of high-fat diet and depends on precursor cell-autonomous TLR4. Further, lean mice exposed to the TLR4 ligand lipopolysaccharide (LPS) at doses similar to that detectable in obese serum recapitulates BM lympho-myeloid alterations. Together, these results establish a mechanistic contribution of BM cell-intrinsic TLR4 to obesity-driven BM malfunction and demonstrate the importance of LPS. Our findings raises important questions about the impact of maternal obesity and endotoxemia to fetal hematopoiesis, as fetal immune precursors are also sensitive to TLR4 signals.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.