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The Link module of human TSG-6 (Link_TSG6) promotes wound healing, suppresses inflammation and improves glandular function in mouse models of Dry Eye Disease

Cited 8 time in Web of Science Cited 8 time in Scopus
Authors

Oh, Joo Youn; Ryu, Jin Suk; Kim, Hyeon Ji; Kouvatsos, Nikolaos; Dodd, Rebecca J.; Choi, Se Hyun; Kim, Yu Jeong; Milner, Caroline M.; Day, Anthony J.

Issue Date
2022-04
Publisher
Ethis Communications
Citation
Ocular Surface, Vol.24, pp.40-50
Abstract
© 2021 The AuthorsPurpose: To investigate the potential of the Link_TSG6 polypeptide comprising the Link module of human TSG-6 (TNF-stimulated gene/protein-6) as a novel treatment for dry eye disease (DED). Methods: We analyzed the therapeutic effects of topical application of Link_TSG6 in two murine models of DED, the NOD.B10.H2b mouse model and the desiccating stress model. The effects of Link_TSG6 on the ocular surface and DED were compared with those of full-length TSG-6 (FL_TSG6) and of 0.05% cyclosporine (Restasis®). Additionally, the direct effect of Link_TSG6 on wound healing of the corneal epithelium was evaluated in a mouse model of corneal epithelial debridement. Results: Topical Link_TSG6 administration dose-dependently reduced corneal epithelial defects in DED mice while increasing tear production and conjunctival goblet cell density. At the highest dose, no corneal lesions remained in ∼50% of eyes treated. Also, Link_TSG6 significantly suppressed the levels of inflammatory cytokines at the ocular surface and inhibited the infiltration of T cells in the lacrimal glands and draining lymph nodes. Link_TSG6 was more effective in decreasing corneal epithelial defects than an equimolar concentration of FL_TSG6. Link_TSG6 was significantly more potent than Restasis® at ameliorating clinical signs and reducing inflammation. Link_TSG6 markedly and rapidly facilitated epithelial healing in mice with corneal epithelial debridement wounds. Conclusion: Link_TSG6 holds promise as a novel therapeutic agent for DED through its effects on the promotion of corneal epithelial healing and tear secretion, the preservation of conjunctival goblet cells and the suppression of inflammation.
ISSN
1542-0124
URI
https://hdl.handle.net/10371/179783
DOI
https://doi.org/10.1016/j.jtos.2021.12.012
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  • College of Medicine
  • Department of Medicine
Research Area 각막 및 외안부 질환, 백내장

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