Claudins (CLs) comprise a multi-gene family functionally involved in the tight junction barrier and aqueous pore formation and thereby play a key role in determining the permeability properties of epithelial cells. In particular, CL-1 is expressed ubiquitously in most tissues of the body, while CL-2 is highly expressed in leaky epithelial tissues, including the intestinal crypts. The aim of this study was to investigate the immunolocalization of CL-1 and CL-2, transmembrane proteins identified as integral components of tight junction strands, in duodenal biopsies of control subjects and in patients with Systemic Nickel Allergy Syndrome (SNAS), characterized by the presence of systemic and gastrointestinal symptoms following nickel ingestion. In parallel the F-actin cytoskeletal organization was assessed in biopsy samples. Staining with rhodamine phalloidin indicated that the junctional protein CL1 and CL2 are membrane cytoskeleton-associated. Confocal microscopic analysis of intestinal sections (5 µm) revealed an increased immunofluorescence signal for both CL1 and CL2 in subject sensitive to nickel sulfate compared to controls. In conclusion CL1 and CL2 showed an increased expression in SNAS patient as assessed by immunofluorescence analysis. This could be associated with alteration of tight junction organization and permeability of the gastrointestinal barrier in SNAS disease
File in questo prodotto:
Non ci sono file associati a questo prodotto.