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MAXINE GOWEN, KAREN CHAPMAN, AMANDA LITTLEWOOD, DAVID HUGHES, DEAN EVANS, GRAHAM RUSSELL, Production of Tumor Necrosis Factor by Human Osteoblasts is Modulated by Other Cytokines, but not by Osteotropic Hormones, Endocrinology, Volume 126, Issue 2, 1 February 1990, Pages 1250–1255, https://doi.org/10.1210/endo-126-2-1250
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Human osteoblast cultures derived as outgrowths from trabecular bone released tumor necrosis factor (TNFα) upon stimulation of the cells with human recombinant interleukin 1 (IL1; 10-13–10-11 M), human recombinant granulocyte-macrophage colony-stimulating factor (100–1000 U/ml), and bacterial lipopolysaccharide (5–500 ng/ml). The osteotropic hormones 1,25-dihydroxyvitamin D3, PTH, and calcitonin had no effect on TNF production. The TNF released by the osteoblasts was identified as TNFα, using a specific anti-TNFα monoclonal antibody to neutralize its activity. Immunohistochemical staining of the cells using the same antibody revealed that all of the cells in the cultures were capable of producing TNFα, including those that also expressed alkaline phosphatase activity. Immunoreactive protein could be detected in the perinuclear region when cells were cultured in the presence of monensin, suggesting accumulation of newly synthesised protein in the Golgi apparatus. These results suggest that human osteoblasts, which have been shown previously to respond to TNFα, can synthesize and release TNF in response to IL1 and granulocyte-macrophage colony-stimulating factor. TNF may, therefore, not only have a pathological role in conditions of chronic inflammation, but also may act as a local paracrine or autocrine regulator of osteoblast function. (Endocrinology126: 1250–1255, 1990)
