Purpose: Inflammation and squamous metaplasia is a common pathological process that occurs in many ocular surface diseases such as dry eye, Stevens-Johnson syndrome, mucous membrane pemphigoid, and chemical/thermal burns. At present, there is no ideal medicinal treatment for this abnormality. We report herein on an ex vivo conjunctival inflammation and squamous metaplasia model by culturing human conjunctival tissues at an air-liquid interface for up to 8 days to study the effects of minocycline on inflammation and squamous metaplasia.
Methods: The levels of inflammatory mediators including interleukin-1β, tumor necrosis factor-α, and metalloproteinase-9 in the cultured human conjunctival tissues were determined by enzyme-linked immuno-sorbent assay and real-time polymerase chain reaction. The total and phosphorylated nuclear factor-κB were detected by western blot. Differentiation markers K10, MUC5AC, and Pax6 and proliferation markers Ki67, p63, and K14 were determined by immunofluorescence or immunohistochemical staining.
Results: The results indicated that minocycline inhibited inflammation, decreased the expression of interleukin-1β, tumor necrosis factor-α, and metalloproteinase -9, and squamous metaplasia features such as hyperproliferation and abnormal epidermal differentiation of conjunctival epithelium.
Conclusions: These findings highlight the possibility that minocycline could be used to treat dry eye and other ocular surface diseases exhibiting epithelial cell inflammation and squamous metaplasia.