Carmela Olivieri1, Elena Bargagli1, Simona Inghilleri2, Ilaria Campo2, Marcella Cintorino3, Paola Rottoli1. 1. a UOC Respiratory Diseases and Lung Transplantation , Department of Internal and Specialist Medicine , University of Siena , Siena , Italy. 2. b Pneumology Unit , IRCCS San Matteo Foundation Hospital , Pavia , Italy. 3. c Section of Pathology , Department of Medical Biotechnology , University of Siena , Siena , Italy.
Abstract
INTRODUCTION: Idiopathic pulmonary fibrosis (IPF) is a severe interstitial lung disorder characterized by a pattern of Usual Interstitial Pneumonia where the presence of fibroblastic foci is the hallmark of the disease. AIM OF THE STUDY: In the present study, we analyzed the migration inhibitory factor (MIF) expression in lung tissue of IPF patients compared with healthy controls and organizing pneumonia (OP) patients focusing into MIF potential role in fibroblastic foci development. MATERIALS AND METHODS: The immunohistochemical analysis was performed in 10 IPF patients (7 male), 3 OP patients (2 male), and 3 healthy controls (all male) using the streptavidin-biotin method (Dako). RESULTS: In IPF samples, MIF resulted overexpressed in the areas of active fibrosis and, in particular, in the alveolar epithelium, bronchiolar epithelium, and in the peripheral zones of fibroblastic foci. Bronchiolar epithelium from organizing pneumonia patients resulted only weakly positive for MIF while no evidence of MIF expression was reported for alveolar epithelium. In the control subject group, MIF was unexpressed except for a weak presence in the bronchiolar epithelium. CONCLUSION: In conclusion, MIF is a pleiotropic cytokine involved in the pathogenesis of IPF being mainly expressed in the areas of remodeling and active fibrosis, in bronchiolar and alveolar epithelium, and in the peripheral zone of fibroblastic foci.
INTRODUCTION:Idiopathic pulmonary fibrosis (IPF) is a severe interstitial lung disorder characterized by a pattern of Usual Interstitial Pneumonia where the presence of fibroblastic foci is the hallmark of the disease. AIM OF THE STUDY: In the present study, we analyzed the migration inhibitory factor (MIF) expression in lung tissue of IPF patients compared with healthy controls and organizing pneumonia (OP) patients focusing into MIF potential role in fibroblastic foci development. MATERIALS AND METHODS: The immunohistochemical analysis was performed in 10 IPF patients (7 male), 3 OP patients (2 male), and 3 healthy controls (all male) using the streptavidin-biotin method (Dako). RESULTS: In IPF samples, MIF resulted overexpressed in the areas of active fibrosis and, in particular, in the alveolar epithelium, bronchiolar epithelium, and in the peripheral zones of fibroblastic foci. Bronchiolar epithelium from organizing pneumoniapatients resulted only weakly positive for MIF while no evidence of MIF expression was reported for alveolar epithelium. In the control subject group, MIF was unexpressed except for a weak presence in the bronchiolar epithelium. CONCLUSION: In conclusion, MIF is a pleiotropic cytokine involved in the pathogenesis of IPF being mainly expressed in the areas of remodeling and active fibrosis, in bronchiolar and alveolar epithelium, and in the peripheral zone of fibroblastic foci.
Authors: Cory Wilson; Tinne Cj Mertens; Pooja Shivshankar; Weizen Bi; Scott D Collum; Nancy Wareing; Junsuk Ko; Tingting Weng; Ram P Naikawadi; Paul J Wolters; Pascal Maire; Soma Sk Jyothula; Rajarajan A Thandavarayan; Dewei Ren; Nathan D Elrod; Eric J Wagner; Howard J Huang; Burton F Dickey; Heide L Ford; Harry Karmouty-Quintana Journal: JCI Insight Date: 2022-05-23
Authors: Peter Luedike; Georgios Alatzides; Maria Papathanasiou; Martin Heisler; Julia Pohl; Nils Lehmann; Tienush Rassaf Journal: Eur J Med Res Date: 2018-05-04 Impact factor: 2.175