ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2019
Attenuation of NF-κB in Intestinal Epithelial Cells Is Sufficient to Mitigate the Bone Loss Comorbidity of Experimental Mouse Colitis.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
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- Regulation of Inducible Nitric Oxide Synthase (NOS2) Expression in Healthy and Inflamed Bowel: A Narrative Review.International journal of molecular sciences · 2026Review
- Dietary supplementation with raw potato starch reversed enteritis-induced bone loss via Malt1 paracaspase inhibition in meat ducks.Poultry science · 2026Article
- Physicochemical properties of raw potato starch and its protective effect on bone quality in meat ducks with enteritis.Poultry science · 2026Article
- Metabolic Disorders and Inflammatory Bowel Diseases: Unraveling Shared Pathways and Clinical Interactions.Metabolites · 2026Review
- Interactions between the gut microbiota and immune cell dynamics: novel insights into the gut-bone axis.Gut microbes · 2025Review
- Synergistic exacerbation of periprosthetic osteolysis by inflammatory bowel disease and titanium ions: Impaired osteogenesis of BMSCs via PI3K/AKT signaling.Materials today. Bio · 2025Article
- Regulatory Mechanisms of Gut Homeostasis and Bone Metabolism Interplay in Osteoporosis.Phenomics (Cham, Switzerland) · 2025Review
- IĸBζ as a Central Modulator of Inflammatory Arthritis Pathogenesis.Arthritis & rheumatology (Hoboken, N.J.) · 2025Article
- Colon-targeted engineered postbiotics nanoparticles alleviate osteoporosis through the gut-bone axis.Nature communications · 2024Article
- Fibrous Dysplasia Masquerading as Sternal Malignancy: A Rare and Challenging Presentation.Cureus · 2023Article
- Microbial Metabolites as Ligands to Xenobiotic Receptors: Chemical Mimicry as Potential Drugs of the Future.Drug metabolism and disposition: the biological fate of chemicals · 2023Review
- ILC3: a case of conflicted identity.Frontiers in immunology · 2023Review
- Compound loss of GSDMD and GSDME function is necessary to achieve maximal therapeutic effect in colitis.Journal of translational autoimmunity · 2022Article
- Loss ofFrontiers in cellular and infection microbiology · 2022Article
- The Rising Era of "Immunoporosis": Role of Immune System in the Pathophysiology of Osteoporosis.Journal of inflammation research · 2022Review
- Intestinal Inflammation Promotes MDL-1Cellular and molecular gastroenterology and hepatology · 2022Article
- RNA-Binding Protein HuR Suppresses Inflammation and Promotes Extracellular Matrix Homeostasis via NKRF in Intervertebral Disc Degeneration.Frontiers in cell and developmental biology · 2020Article
- Mechanisms Underlying Bone Loss Associated with Gut Inflammation.International journal of molecular sciences · 2019Review
- Critical Roles of Balanced Innate Lymphoid Cell Subsets in Intestinal Homeostasis, Chronic Inflammation, and Cancer.Journal of immunology research · 2019Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Skeletal abnormalities are common comorbidities of inflammatory bowel disease (IBD). Patients suffering from IBD, including ulcerative colitis and Crohn's disease, present with skeletal complications. However, the mechanism underpinning IBD-associated bone loss remains vague. Intestinal inflammation generates an inflammatory milieu at the intestinal epithelium that leads to dysregulation of mucosal immunity through gut-residing innate lymphoid cells (ILCs) and other cell types. ILCs are recently identified mucosal cells considered as the gatekeeper of gut immunity and their function is regulated by intestinal epithelial cell (IEC)-secreted cytokines in response to the inflammatory microenvironment. We first demonstrate that serum as well as IECs collected from the intestine of dextran sulfate sodium (DSS)-induced colitis mice contain high levels of inflammatory and osteoclastogenic cytokines. Mechanistically, heightened inflammatory response of IECs was associated with significant intrinsic activation of NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) in IECs and increased frequency of ILC1, ILC3, and myeloid osteoclast progenitors. Validating the central role of IEC-specific NF-κB activation in this phenomenon, conditional expression of constitutively active inhibitor kappa B kinase 2 (IKK2) in IECs in mice recapitulates the majority of the cellular, inflammatory, and osteolytic phenotypes observed in the chemically induced colitis. Furthermore, conditional deletion of IKK2 from IECs significantly attenuated inflammation and bone loss in DSS-induced colitis. Finally, using the DSS-induced colitis model, pharmacologic inhibition of IKK2 was effective in reducing frequency of ILC1 and ILC3 cells, attenuated circulating levels of inflammatory cytokines, and halted colitis-associated bone loss. Our findings identify IKK2 in IECs as viable therapeutic target for colitis-associated osteopenia.
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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.