Tumor necrosis factor alpha ($TNF{alpha}$) is a multifunctional inflammatory cytokine that regulates various cellular and biological processes. Increased levels of $TNF{alpha}$ have been implicated in a number of human diseases including diabetes and arthritis. Sympathetic nervous system stimulation via the beta2-adrenergic receptor (${eta}2AR$) in osteoblasts suppresses osteogenic activity. We previously reported that $TNF{alpha}$ upregulates ${eta}2AR$ expression in murine osteoblastic cells and that this modulation is associated with $TNF{alpha}$ inhibition of osteoblast differentiation. In our present study, we explored whether $TNF{alpha}$ induces ${eta}2AR$ expression in human osteoblasts and then identified the downstream signaling pathway. Our results indicated that ${eta}2AR$ expression was increased in Saos-2 and C2C12 cells by $TNF{alpha}$ treatment, and that this increase was blocked by the inhibition of NF-${kappa}B$ activation. Chromatin immunoprecipitation and luciferase reporter assay results indicated that NF-${kappa}B$ directly binds to its cognate elements on the ${eta}2AR$ promoter and thereby stimulates ${eta}2AR$ expression. These findings suggest that the activation of $TNF{alpha}$ signaling in osteoblastic cells leads to an upregulation of ${eta}2AR$ and also that $TNF{alpha}$ induces ${eta}2AR$ expression in an NF-${kappa}B$-dependent manner.