PAR-2, IL-4R, TGF-β and TNF-α in bronchoalveolar lavage distinguishes extrinsic allergic alveolitis from sarcoidosis
Status PubMed-not-MEDLINE Jazyk angličtina Země Řecko Médium print-electronic
Typ dokumentu časopisecké články
PubMed
25009615
PubMed Central
PMC4079423
DOI
10.3892/etm.2014.1776
PII: etm-08-02-0533
Knihovny.cz E-zdroje
- Klíčová slova
- extrinsic allergic alveolitis, interleukin-4 receptor, proteinase-activated receptor-2, sarcoidosis, transforming growth factor-β, tumor necrosis factor-α,
- Publikační typ
- časopisecké články MeSH
Sarcoidosis (SARC) and extrinsic allergic alveolitis (EAA) share certain markers, making a differential diagnosis difficult even with histopathological investigation. In lung tissue, proteinase-activated receptor-2 (PAR-2) is primarily investigated with regard to epithelial and inflammatory perspectives. Varying levels of certain chemokines can be a useful tool for distinguishing EAA and SARC. Thus, in the present study, differences in the levels of transforming growth factor (TGF)-β1, tumor necrosis factor (TNF)-α, interleukin-4 receptor (IL-4R) and PAR-2 in bronchoalveolar lavage fluid (BALF) were compared, using an ELISA method, between 14 patients with EAA and six patients with SARC. Statistically significant higher levels of IL-4R, PAR-2 and the PAR-2/TGF-β1 and PAR-2/TNF-α ratios were observed in EAA patients as compared with SARC patients. Furthermore, the ratios of TNF-α/total protein, TGF-β1/PAR-2 and TNF-α/PAR-2 were significantly lower in EAA patients than in SARC patients. The results indicated a higher detection of PAR-2 in EAA samples in association with TNF-α and TGF-β levels. As EAA and PAR-2 in parallel belong to the Th2-mediated pathway, the results significantly indicated an association between this receptor and etiology. In addition, the results indicated that SARC is predominantly a granulomatous inflammatory disease, thus, higher levels of TNF-α are observed. Therefore, the detection of PAR-2 and investigated chemokines in BALF may serve as a useful tool in the differential diagnosis between EAA and SARC.
Department of Pathology and Molecular Medicine Thomayer Hospital Prague 140 59 Czech Republic
Department of Respiratory Medicine Thomayer Hospital Prague 140 59 Czech Republic
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Facco M, Cabrelle A, Teramo A, et al. Sarcoidosis is a Th1/Th17 multisystem disorder. Thorax. 2011;66:144–150. PubMed
Mitaka K, Miyazaki Y, Yasui M, et al. Th2-biased immune responses are important in a murine model of chronic hypersensitivity pneumonitis. Int Arch Allergy Immunol. 2011;154:264–274. PubMed
Barrera L, Mendoza F, Zuñiga J, et al. Functional diversity of T-cell subpopulations in subacute and chronic hypersensitivity pneumonitis. Am J Respir Crit Care Med. 2008;177:44–55. PubMed
van der Poll T, de Boer JD, Levi M. The effect of inflammation on coagulation and vice versa. Curr Opin Infect Dis. 2011;24:273–278. PubMed
Petäjä J. Inflammation and coagulation. An overview Thromb Res. 2011;127(Suppl 2):S34–S37. PubMed
Déry O, Corvera CU, Steinhoff M, Bunnett NW. Proteinase-activated receptors: novel mechanisms of signaling by serine proteases. Am J Physiol. 1998;274:C1429–C1452. PubMed
Macfarlane SR, Seatter MJ, Kanke T, et al. Proteinase-activated receptors. Pharmacol Rev. 2001;53:245–282. PubMed
Leger AJ, Covic L, Kuliopulos A. Protease-activated receptors in cardiovascular diseases. Circulation. 2006;114:1070–1077. PubMed
Boitano S, Flynn AN, Sherwood CL, et al. Alternaria alternata serine proteases induce lung inflammation and airway epithelial cell activation via PAR2. Am J Physiol Lung Cell Mol Physiol. 2011;300:L605–L614. PubMed PMC
Matěj R, Vašáková M, Kukal J, Sterclová M, Olejár T. Higher TGF-β with lower CD124 and TSLP, but no difference in PAR-2 expression in bronchial biopsy of bronchial asthma patients in comparison with COPD patients. Appl Immunohistochem Mol Morphol. 2013 Oct 31; (Epub ahead of print) PubMed
Vasakova M, Sterclova M, Matej R, et al. IL-4 polymorphisms, HRCT score and lung tissue markers in idiopathic pulmonary fibrosis. Hum Immunol. 2013;74:1346–1351. PubMed
Kouzaki H, O‘Grady SM, Lawrence CB, Kita H. Proteases induce production of thymic stromal lymphopoietin by airway epithelial cells through protease-activated receptor-2. J Immunol. 2009;183:1427–1434. PubMed PMC
Ito T, Wang YH, Duramad O, et al. TSLP-activated dendritic cells induce an inflammatory T helper type 2 cell response through OX40 ligand. J Exp Med. 2005;202:1213–1223. PubMed PMC
Wang YH, Ito T, Wang YH, et al. Maintenance and polarization of human TH2 central memory T cells by thymic stromal lymphopoietin-activated dendritic cells. Immunity. 2006;24:827–838. PubMed
Wallace WA, Howie SE. Immunoreactive interleukin 4 and interferon-gamma expression by type II alveolar epithelial cells in interstitial lung disease. J Pathol. 1999;187:475–480. PubMed
Wygrecka M, Kwapiszewska G, Jablonska E, et al. Role of protease-activated receptor-2 in idiopathic pulmonary fibrosis. Am J Respir Crit Care Med. 2011;183:1703–1714. PubMed
Materazzi S, Pellerito S, Di Serio C, et al. Analysis of protease-activated receptor-1 and -2 in human scar formation. J Pathol. 2007;212:440–449. PubMed
Higashimoto Y, Yamagata Y, Taya S, et al. Systemic inflammation in chronic obstructive pulmonary disease and asthma: Similarities and differences. Respirology. 2008;13:128–133. PubMed
Szlubowski A, Soja J, Grzanka P, et al. TGF-beta1 in bronchoalveolar lavage fluid in diffuse parenchymal lung diseases and high-resolution computed tomography score. Pol Arch Med Wewn. 2010;120:270–275. PubMed
Mohr LC. Hypersensitivity pneumonitis. Curr Opin Pulm Med. 2004;10:401–411. PubMed
Dai H, Guzman J, Chen B, Costabel U. Production of soluble tumor necrosis factor receptors and tumor necrosis factor-alpha by alveolar macrophages in sarcoidosis and extrinsic allergic alveolitis. Chest. 2005;127:251–256. PubMed
Nhu QM, Shirey KA, Pennini M, et al. Protease-activated receptor 2 activation promotes an anti-inflammatory and alternatively activated phenotype in LPS-stimulated murine macrophages. Innate Immun. 2012;18:193–203. PubMed PMC
Ebeling C, Lam T, Gordon JR, et al. Proteinase-activated receptor-2 promotes allergic sensitization to an inhaled antigen through a TNF-mediated pathway. J Immunol. 2007;179:2910–2917. PubMed
No authors listed. Statement on sarcoidosis. Am J Respir Crit Care Med; Joint Statement of the American Thoracic Society (ATS), the European Respiratory Society (ERS) and the World Association of Sarcoidosis and Other Granulomatous Disorders (WASOG) adopted by the ATS Board of Directors and by the ERS Executive Committee; February 1999; 1999. pp. 736–755. PubMed
Chignard M, Pidard D. Neutrophil and pathogen proteinases versus proteinase-activated receptor-2 lung epithelial cells: more terminators than activators. Am J Respir Cell Mol Biol. 2006;34:394–398. PubMed
Armstrong L, Godinho SI, Uppington KM, et al. Tumour necrosis factor-alpha processing in interstitial lung disease: a potential role for exogenous proteinase-3. Clin Exp Immunol. 2009;156:336–343. PubMed PMC
Vliagoftis H, Schwingshackl A, Milne CD, et al. Proteinase-activated receptor-2-mediated matrix metalloproteinase-9 release from airway epithelial cells. J Allergy Clin Immunol. 2000;106:537–545. PubMed
Perng DW, Chang KT, Su KC, et al. Matrix metalloprotease-9 induces transforming growth factor-β(1) production in airway epithelium via activation of epidermal growth factor receptors. Life Sci. 2011;89:204–212. PubMed
Lewkowich IP, Day SB, Ledford JR, et al. Protease-activated receptor 2 activation of myeloid dendritic cells regulates allergic airway inflammation. Respir Res. 2011;12:122. PubMed PMC
Antoniu SA. Targeting the TNF-alpha pathway in sarcoidosis. Expert Opin Ther Targets. 2010;14:21–29. PubMed
Costabel U. The alveolitis of hypersensitivity pneumonitis. Eur Respir J. 1988;1:5–9. PubMed