IMMUNOHISTOCHEMICAL STUDY OF E-CADHERIN AND ZO-1 IN ALLERGIC NASAL EPITHELIUM OF THE GUINEA-PIG

Nasal epithelial damage during allergic inflammation was studied by ob serving the distribution of cell adhesion molecule E-cadherin and tigh t junction (zonula occludens) cell-cell contact associated protein ZO- 1, The guinea pig model of nasal allergy, sensitized with intraperiton eally administered ovalbumin (OA) and subsequently challenged with OA intranasally, was used. In control epithelium, E-cadherin immunoreacti vity was detected continuously along neighboring epithelial cell borde rs. ZO-1 spot-like immunoreactivity was detected in the apicolateral p ortion of epithelial cells corresponding to the tight junction (TJ) po sition, but no changes in immunoreactivity were found between control and challenged epithelia. In the challenged epithelium of sensitized a nimals, marked infiltration eosinophils and structural changes, such a s widening of the intercellular spaces and detachment of adjacent epit helial cells, were observed concurrently. In addition. spots negative for E-cadherin immunoreactivity were noted in the epithelium, associat ed with the extracellular deposition of eosinophil granule proteins. I mmunoelectron microscopy revealed a decrease or disappearance of E-cad herin immunoreactivity, which took place not only in regions where int ercellular spaces were wide and adjacent epithelial cells were detache d, but also at the point of contact between infiltrating eosinophils a nd epithelial cells. Approximately 87% of eosinophils observed in the challenged epithelium were associated with such loss of E-cadherin imm unoreactivity. These results suggest that the intimate epithelial cell contact mediated by E-cadherin is loosened as a consequence of eosino phil infiltration, which may trigger the initial step of subsequent ep ithelial destruction in allergic states.