Idiopathic pulmonary fibrosis: immunohistochemical analysis provides fresh insights into lung tissue remodelling with implications for novel prognostic markers

This study explored the cellular and biological interrelationships involved in Idiopathic Pulmonary Fibrosis (IPF) lung tissue remodelling using immunohistochemical analysis. IPF and control lung tissues were examined for localisation of Epithelial Mesenchymal Transition (EMT), proliferation and gro...

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Published in:International journal of clinical and experimental pathology 2012-01, Vol.5 (1), p.58-71
Main Authors: Lomas, Nicola J, Watts, Keira L, Akram, Khondoker M, Forsyth, Nicholas R, Spiteri, Monica A
Format: Article
Language:English
Subjects:
Epithelial-Mesenchymal Transition - physiology
Humans
Idiopathic Pulmonary Fibrosis - metabolism
Idiopathic Pulmonary Fibrosis - pathology
Immunohistochemistry
Original
Prognosis
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creator Lomas, Nicola J
Watts, Keira L
Akram, Khondoker M
Forsyth, Nicholas R
Spiteri, Monica A
description This study explored the cellular and biological interrelationships involved in Idiopathic Pulmonary Fibrosis (IPF) lung tissue remodelling using immunohistochemical analysis. IPF and control lung tissues were examined for localisation of Epithelial Mesenchymal Transition (EMT), proliferation and growth factor markers assessing their relationship to key histological aberrations. E-cadherin was expressed in IPF and control (Alveolar type II) ATII cells (>75%). In IPF, mean expression of N-cadherin was scanty (75%); cytoplasmic collagen I in ATII cells was present in 3 IPF cases. IPF ATII cells demonstrated variable Surfactant Protein-C (SP-C). The pathogenesis of IPF is complex and involves multiple factors, possibly including EMT. Histological analysis suggests TGF-β-stimulated myofib rob lasts initiate a contractile response within established fibroblastic foci while proliferating ATII cells attempt to instigate alveolar epithelium repair. Marker expression (N-cadherin and Ki-67) correlation with histological disease activity (as reflected by fibroblastic foci extent) may emerge as future prognostic indicators for IPF.
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IPF ATII cells demonstrated variable Surfactant Protein-C (SP-C). The pathogenesis of IPF is complex and involves multiple factors, possibly including EMT. Histological analysis suggests TGF-β-stimulated myofib rob lasts initiate a contractile response within established fibroblastic foci while proliferating ATII cells attempt to instigate alveolar epithelium repair. Marker expression (N-cadherin and Ki-67) correlation with histological disease activity (as reflected by fibroblastic foci extent) may emerge as future prognostic indicators for IPF.</abstract><cop>United States</cop><pub>e-Century Publishing Corporation</pub><pmid>22295148</pmid><tpages>14</tpages></addata></record>
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subjects Epithelial-Mesenchymal Transition - physiology
Humans
Idiopathic Pulmonary Fibrosis - metabolism
Idiopathic Pulmonary Fibrosis - pathology
Immunohistochemistry
Original
Prognosis
title Idiopathic pulmonary fibrosis: immunohistochemical analysis provides fresh insights into lung tissue remodelling with implications for novel prognostic markers
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