Endothelin-1 (ET-1), a potent
vasoconstrictor peptide, is involved in several functions of eye pathophysiology, such as regulation of intraocular tension and
retinal reactive vasoconstriction. As ET-1 pro-inflammatory and fibrosing activity is emerging in different fields of pathology, we investigated the expression of ET-1 and
endothelin-converting enzyme-1 (ECE-1) in
chalazia, granulomatous lesions of the eyelid. ET-1 and ECE-1 were analyzed by immunohistochemistry (IHC) in twenty surgically removed
chalazia, with regard to expression in eyelid structures and inflammatory infiltrate. Phenotype of ET-1 expressing inflammatory cells was established by double immunofluorescence. The cellular localization of prepro-ET-1 (pp-ET-1)
mRNA and ECE-1
mRNA was studied by nonisotopic in situ hybridization (ISH). Neutrophils (PMNs), macrophages and T-lymphocytes were scattered in stroma, around alveoli and grouped in lipogranulomas. PMNs, macrophages, basal epithelium of meibomian adenomers and central ducts immunostained for ET-1. ECE-1
protein was found in meibomian adenomers, conjunctival epithelium, tarsal mucous glands and in inflammatory cells. Hybridization signals for pp-ET-1
mRNA and ECE-1
mRNA were recognized in healthy and degenerating meibomian ducts, adenomers, inflammatory cells, as well as in vessel walls. ECE-1
mRNA was also present in conjunctival epithelium and Henle's crypts. Our findings suggest that the multifunctional
peptide ET-1 may have a role in molecular genesis of tissue damage in
chalazia. ET-1
cytokine activity is likely to support the migration of inflammatory cells and the setting of lipogranulomas; ET-1 stimulation might contribute to proliferation of fibroblasts and
collagen synthesis. ET-1 upregulation on meibomian adenomers and ducts may further enhance
granulomas formation by stimulating
lipid release.