Annals of Thoracic Medicine Official publication of the Saudi Thoracic Society, affiliated to King Saud University
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Year : 2013  |  Volume : 8  |  Issue : 1  |  Page : 38-45

Multiplex protein profiling of bronchoalveolar lavage in idiopathic pulmonary fibrosis and hypersensitivity pneumonitis

1 Department of Pathophysiology, Katholieke Universiteit Leuven and University Hospital Gasthuisberg, Leuven, Belgium
2 Department of Histology, Katholieke Universiteit Leuven and University Hospital Gasthuisberg, Leuven, Belgium

Correspondence Address:
A Wuyts Wim
Department of Pathophysiology, Katholieke Universiteit Leuven, Laboratory of Pneumology, Interstitial Lung Disease Unit, Herestraat 49 Bus 706, B-3000 Leuven
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Source of Support: Wim Wuyts is a Senior Clinical Investigator of the Research Foundation - Flanders: 1.8.325.12N. Stijn Willems is research fellow of the Agency for Innovation by Science and Technology in Flanders (IWT) and Bart Vanaudenaerde is a senior research fellow of the FWO. Geert M Verleden is holder of the GSK (Belgium) chair in respiratory pharmacology at the Katholieke Universiteit Leuven (KUL), and is supported by grants from the KUL (OT/050/10) and the FWO.Flanders: G.0643.08 and G.0723.10., Conflict of Interest: None

DOI: 10.4103/1817-1737.105718

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Context: Idiopathic pulmonary fibrosis (IPF) and chronic hypersensitivity pneumonitis (HP) are diffuse parenchymal lung diseases characterized by a mixture of inflammation and fibrosis, leading to lung destruction and finally death. AIMS: The aim of this study was to compare different pathophysiological mechanisms, such as angiogenesis, coagulation, fibrosis, tissue repair, inflammation, epithelial damage, oxidative stress, and matrix remodeling, in both disorders using bronchoalveolar lavage (BAL). Methods: At diagnosis, patients underwent bronchoscopy with BAL and were divided into three groups: Control ( n = 10), HP ( n = 11), and IPF ( n = 11), based on multidisciplinary approach (clinical examination, radiology, and histology): Multiplex searchlight technology was used to analyze 25 proteins representative for different pathophysiological processes: Eotaxin, basic fibroblast growth factor (FGFb), fibronectin, hepatocyte growth factor (HGF), interleukine (IL)-8, IL-12p40, IL-17, IL-23, monocyte chemotactic protein (MCP-1), macrophage-derived chemokine (MDC), myeloperoxidase (MPO), matrix metalloproteinase (MMP)-8, MMP-9, active plasminogen activating inhibitor 1 (PAI-1), pulmonary activation regulated chemokine (PARC), placental growth factor (PlGF), protein-C, receptor for advanced glycation end products (RAGE), regulated on activation normal T cells expressed and secreted (RANTES), surfactant protein-C (SP-C), transforming growth factor-β1 (TGF-β1), tissue inhibitor of metalloproteinase-1 (TIMP-1), tissue factor, thymic stromal lymphopoietin (TSLP), and vascular endothelial growth factor (VEGF). Results: All patients suffered from decreased pulmonary function and abnormal BAL cell differential compared with control. Protein levels were increased in both IPF and HP for MMP-8 ( P = 0.022), MMP-9 ( P = 0.0020), MCP-1 ( P = 0.0006), MDC ( P = 0.0048), IL-8 ( P = 0.013), MPO ( P = 0.019), and protein-C ( P = 0.0087), whereas VEGF was decreased ( P = 0.0003) compared with control. HGF was upregulated in HP ( P = 0.0089) and active PAI-1 was upregulated ( P = 0.019) in IPF compared with control. Differences in expression between IPF and HP were observed for IL-12p40 ( P = 0.0093) and TGF-β1 ( P = 0.0045). Conclusions: Using BAL, we demonstrated not only expected similarities but also important differences in both disorders, many related to the innate immunity. These findings provide new clues for further research in both disorders.

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