PURPOSE: Lymphangiogenesis has been reported to be driven by mediators (e.g hyaluronic acid) and inflammatory cells (e.g activated CD11b+ macrophages), both commonly met in COPD. We hypothesized that lymphangiogenesis is part of COPD pathogenesis. This study aims to investigate the lymphangiogenetic expression in COPD measuring the lymphatic microvessel density (LMVD) and the correlation with the presence of lymphatic invasion(L.I), clinical and laboratory parameters.
METHODS: Lung surgical specimens from 20 smokers [10 COPD-smokers (30% stage 2 GOLD) and 10 non-COPD smokers] with mean age of 62.6 years (range 38-82) were immunohistochemically stained for D2-40 and LYVE-1. Calculation of LMVD and assessment of L.I were performed and correlation with clinical and spirometric data followed.
RESULTS: D2-40 and LYVE-1 were expressed in all specimens presenting higher expression (LMVD) in COPD-smokers (p=0.00). L.I was presented in all COPD specimens. D2-40 and LYVE-1 LMVD were associated with the presence of COPD (x2=20, p<0.001), smoking status (t=-1.8, p=0.09), and disease severity (GOLD)(p=0.00).
CONCLUSION: D2-40 and LYVE-1 being selective lymphatic endothelial markers were highly expressed in COPD specimens in comparison with non-COPD smokers and associated with clinical and spirometric data.
CLINICAL IMPLICATIONS: Our results reported for the first time the presence of newly formed lymphatic vessels in COPD, thus providing a novel insight in the pathogenesis of COPD including lymphangiogenesis.
DISCLOSURE: Georgia Hardavella, No Financial Disclosure Information; No Product/Research Disclosure Information