Wei Li, Chun Chen, Zhiwei Jia, Xuedong Bai and Dike Ruan
Department of Orthopedics, Navy General Hospital, Beijing 100048, China
Introduction: The debilitating effects of lower back pain are a major health issue worldwide. A variety of factors contribute to this, and oftentimes intervertebral disk degeneration (IDD) is an underlying cause of this disorder. Inflammation contributes to IDD, and inflammatory cytokines play key roles in the pathology of IDD. This study characterized the potential to suppress inflammatory cytokine production in degenerative intervertebral disc (NP) cells by treatment with IL-10 and TGF-β in a canine model of IDD.
Methods: IDD was induced surgically in six male beagles, and degenerative NP cells were isolated and cultured for in vitro studies on cytokine production. Cultured degenerative NP cells were divided into four experimental treatment groups: untreated control, IL-10-treated, TGF-β-treated, and IL-10- plus TGF-β-treated cells. Cultured normal NP cells served as a control group. TNF-α expression was evaluated by FACS analysis and ELISA; moreover, ELISA and realtime PCR were also performed to evaluate the effect of IL-10 and TGF-β on NP cell cytokine expression in vitro.
Results: The major findings of these analysis are that after treatment with IL-10 and TGF-β, the expression of extracellular and intracellular TNF-α and IL-1β was suppressed, while the expression of inflammatory cytokines in untreated normal NP cells was significantly lower than that in untreated degenerative NP cells. Our results demonstrated that IL-10 and TGF-β treatment suppressed the expression of IL-1β and TNF-α and inhibited the development of inflammatory responses.
Discussion: We observed that either TGF-β or IL-10 alone suppressed the expression of inflammatory cytokines. Furthermore, their combined use produced a higher level of inhibition of TNF-α and IL-1β than either TGF-β or IL-10 alone. IL-10 and TGF-β should be evaluated as therapeutic approaches for the treatment of lower back pain mediated by IDD.