Purchase this article with an account.
G. Sosne, M. Wheater, P. Qiu, P. Christopherson; Thymosin Beta 4 Inhibits Neutrophil Production of Cytokines After TNF-Alpha Stimulation. Invest. Ophthalmol. Vis. Sci. 2007;48(13):3649.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
The purpose of this study was to investigate the effects of Thymosin ß4 on PMN adhesion to endothelium and cytokine production after TNF-α stimulation
Human PMN were isolated from blood samples from healthy volunteers. Recombinant TNF-α was used to stimulate PMNs with and without Thymosin ß4 and ELISA was performed on cell culture media for IL-1ß and IL-8 at various time points from 0-24 hours. In addition, HUVEC cells were cultured and stimulated with TNF-α with and without Thymosin ß4 and membrane ICAM-1 levels were assayed by ELISA. PMN adhesion to HUVEC was also analyzed when HUVEC cells were co-cultured with PMN in the absence and presence of Thymosin ß4.
Thymosin ß4 significantly decreased PMN expression of IL-1ß and IL-8 after TNF-α stimulation. Thymosin ß4 also decreased membrane ICAM-1 levels in HUVEC and inhibited PMN adhesion to HUVEC.
We have previously demonstrated that Thymosin ß4 is a potent anti-inflammatory agent by inhibiting corneal PMN infiltration and decreasing cytokine, chemokine and MMP-9 production in the setting of alkali injury. From this study, we conclude that Thymosin ß4 may function to inhibit PMN infiltration by decreasing adhesion molecule expression and by suppressing PMN cytokine and chemokine expression. These findings may have clinical therapeutic relevance for the treatment of corneal inflammatory disorders.
This PDF is available to Subscribers Only