Abstract
Purpose: :
Epithelial cells participate in ocular surface defense, among other mechanisms, by acting as a mechanical barrier that prevents intrusion of damaging substances. The integrity of this epithelial barrier is preferentially altered in some ocular surface diseases. The aim of this study was to determine the effect of different cytokine environments (Th1– or Th2–derived) on the expression of several intercellular adhesion proteins in human conjunctival epithelial cells.
Methods: :
The IOBA–NHC cell line, derived from healthy human conjunctival epithelium, was used. The expression of two inflammatory markers (ICAM–1, HLA–DR) and three epithelial intercellular junction proteins: ZO–1 as a marker of tight junctions; desmoplakin (DPK) I–II as a marker of desmosomes; and connexin 43 (Cx 43) as a marker of gap junctions, were analyzed in cells after 48 h incubation with Th1–derived (IFN–γ, or TNF–α) or Th2–derived (IL–4 or IL–13) cytokines by immunofluorescence and Western blotting.
Results: :
ICAM–1 expression, present in basal conditions, was upregulated under stimulation with Th1 or Th2–type cytokines. HLA–DR expression was not detected. IL–4 and IL–13 diminished the expression of ZO–1, DPK I–II, and Cx 43, whereas IFN–γ and TNF–α enhanced that expression.
Conclusions: :
Th2– but not Th1–type cytokines seem to disrupt ocular surface epithelial barrier. This different pattern of epithelial alteration depending on the type of cytokine preponderance may help explain the preferential presence of epithelial ulceration in certain ocular surface problems. If functional studies corroborated these findings, ocular surface epithelial cells would have to be considered as therapeutic targets of new anti–inflammatory medications.
Keywords: conjunctiva • cell adhesions/cell junctions