The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
IL-1 mediates TNF-induced osteoclastogenesis
Open accessAbstract
TNF-induced receptor activator NF-kappaB ligand (RANKL) synthesis by bone marrow stromal cells is a fundamental component of inflammatory osteolysis. We found that this process was abolished by IL-1 receptor antagonist (IL-1Ra) or in stromal cells derived from type I IL-1 receptor-deficient (IL-1RI-deficient) mice. Reflecting sequential signaling of the cytokines TNF and IL-1, TNF induces stromal cell expression of IL-1 and IL-1RI. These data suggest that TNF regulates RANKL expression via IL-1, and, therefore, IL-1 plays a role in TNF-induced periarticular osteolysis. Consistent with this posture, TNF-stimulated osteoclastogenesis in cultures consisting of WT marrow macrophages and stromal cells exposed to IL-1Ra or in cocultures established with IL-1RI-deficient stromal cells was reduced approximately 50%. The same magnitude of osteoclast inhibition occurred in IL-1RI-deficient mice following TNF administration in vivo. Like TNF, IL-1 directly targeted osteoclast precursors and promoted the osteoclast phenotype in a TNF-independent manner in the presence of permissive levels of RANKL. IL-1 is able to induce RANKL expression by stromal cells and directly stimulate osteoclast precursor differentiation under the aegis of p38 MAPK. Thus, IL-1 mediates the osteoclastogenic effect of TNF by enhancing stromal cell expression of RANKL and directly stimulating differentiation of osteoclast precursors.
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The gut microbiota--masters of host development and physiology
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Estrogen deficiency and bone loss: an inflammatory tale
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The gut microbiota regulates bone mass in mice
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Metadata
- Authors
- Wei, S., Kitaura, H., Zhou, P., Ross, F. P., & Teitelbaum, S. L.
- Venue
- Journal of Clinical Investigation
- Published
- 2005-01-20
- Volume
- 115
- Issue
- 2
- Pages
- 282-290
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W1981803131
- Cited by
- 795
- References
- 6
- FWCI
- 17.52
- Type
- journal article
- Language
- en
- Open access
- bronze
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