interleukin-8 and vanadium-pentoxide

Recently it has been hypothesized that vanadium serves a carcinogenic role in the thyroid. However, to date, no in vivo or in vitro studies have evaluated thyroid disruption in humans and/or animals following exposure to vanadium. The present study evaluated the effect of vanadium pentoxide (V2O5) on cell viability and proliferation, and chemokine (C‑X‑C motif) ligand (CXCL)8 and CXCL11 secretion in normal thyrocytes. The results demonstrated that V2O5 had no effect on thyroid follicular cell viability and proliferation. However, V2O5 was able to induce the secretion of CXCL8 and CXCL11 chemokines from thyrocytes. Notably, V2O5 synergistically increased the effect of the interferon (IFN)‑γ on CXCL11 secretion. In addition, V2O5 synergistically increased the effect of tumor necrosis factor‑α on CXCL8 secretion, and abolished the inhibitory effect of IFN‑γ. Overall this induction of CXCL8 and CXCL11 secretion may lead to the induction and perpetuation of an inflammatory reaction in the thyroid. Further studies are now required to evaluate thyroid function and nodule development in subjects who are occupationally exposed, or living in polluted areas.

Topics: Adult; Cell Proliferation; Cell Survival; Cells, Cultured; Chemokine CXCL11; Female; Humans; Inflammation; Interleukin-8; Male; Middle Aged; Thyroid Gland; Vanadium Compounds; Young Adult

An increase in skin rashes or atopic dermatitis has been observed in individuals working with vanadium. However, to the best of our knowledge no in vivo or in vitro studies have evaluated the effect of exposure to vanadium in dermal fibroblasts. Cells viability and proliferation were assessed by WST‑1 assay, cells were treated with increasing concentrations of V2O5 (1, 10 and 100 nM). CXCL8 and CXCL11 concentrations were measured in the supernatants using an ELISA assay. V2O5 was not observed as having a significant effect on dermal fibroblast's viability and proliferation. However, it was revealed that V2O5 was able to induce the secretion of CXCL8 and CXCL11 chemokines into dermal fibroblasts. V2O5 synergistically increased the effect of interferon (IFN)γ on CXCL11 secretion. In addition, V2O5 synergistically increased the effect of the tumor necrosis factor α on CXCL8 secretion and abolished the inhibitory effect of IFNγ. V2O5 induction of CXCL8 and CXCL11 chemokines may lead to the appearance and perpetuation of an inflammatory reaction into the dermal tissue. Further studies are required to evaluate dermal integrity and manifestations in subjects occupationally exposed, or living in polluted areas.

Topics: Aged; Cell Proliferation; Chemokine CXCL11; Female; Fibroblasts; Gene Expression Regulation; Humans; Inflammation; Interferon-gamma; Interleukin-8; Middle Aged; Vanadium Compounds