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Immunohistological studies on lymphatics’ topography in human peripheral nerve are few and recent. By D2-40 immunohistochemistry, we previously described lymphatics in epineurium of human sural nerve. Lymphangiogenesis is described in inflammation. In angiopathic and vasculitic neuropathies proliferation of epineurial blood capillaries is reported. The aim of our study is therefore to investigate the topography and the density of lymphatics in human peripheral nerve and to search possible correlation with blood capillary neovascularization in different neuropathies. We examined biopsied sural nerves of patients suffering from CIDP (chronic inflammatory demyelinating polyneuropathy), vasculitic neuropathy and non inflammatory axonal neuropathy. Immunohistochemistry for detection of lymphatic marker podoplanin (D2-40 antibody) and for general endothelial marker CD31, as well as for Schwann cells protein S-100, was carried out on serial cryostat sections. Morphometric analysis was performed. Lymphatic capillaries were detected in epineurium, most consistently in adjacency of main blood vessels. Occasionally lymphatics were dilated and repleted with mononuclear cells. Podoplanin was also expressed by perineurium and by Schwann cells. No lymphatics were observed endoneurially. Lymphatics showed a far lesser density than blood capillaries and increase of epineurial vascularization resulted significantly associated with higher density of lymphatics. Density variations of epineurial lymphatics, accompanying blood capillaries proliferation, suggest that lymphangiogenesis may occur in neuropathies, in response to inflammation/ischaemia. Lymphatics’ responsiveness to molecular microenvironment is indicated by their expression of growth factor receptors, such as VEGFR3. Lack of lymphatics in closed endoneurial environment is in agreement with analogous findings in brain. Non lymphatic expression of podoplanin is reported in several cell types of nervous system: normal and tumoral ependymal cells, perineurium and Schwann cells. As biological functions of podoplanin, involved in cell migration and cytoskeletal reorganization, are uncompletely understood, its localization on non lymphatic structures of peripheral nerve needs to be defined., Italian Journal of Anatomy and Embryology, Vol 117, No 2 (Supplement) 2012

Lymphatics were detected in the epineurium of the human sural nerve by D-240 immunostaining and confirmed by ultrastructural examination.

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 Tlymphocytes 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.