Eosinophil Inflammation of Nasal Polyp Tissue: Relationships with Matrix Metalloproteinases, Tissue Inhibitor of Metalloproteinase-1, and Transforming Growth Factor-beta1

Abstract

Eosinophil and mast cell infiltrations are consistent findings in nasal polyp tissue. Previous studies have shown that matrix metalloproteinases (MMPs) may be involved in eosinophil infiltration in airway mucosa of asthmatic patients, and that transforming growth factor-beta1 (TGF-beta1) induces extracellular matrix deposition in nasal polyp tissue. The aim of this study was to evaluate the role of MMPs and tissue-inhibitor of metalloproteinase-1 (TIMP-1) in association with TGF-beta1, eosinophils and mast cell activation in nasal polyp tissue. Nasal polyp tissues from 20 patients who underwent polypectomies were collected and prepared into tissue homogenate. Eosinophil cationic protein (ECP) and tryptase levels were measured by CAP system (Pharmacia, Sweden). MMP-2, MMP-9, TIMP-1 and TGF-beta1 levels were measured by enzyme-liked immunosorbent assay. MMP-2 was the predominant form of MMPs, followed by MMP-9 and TIMP-1. There were significant correlations between ECP, and MMP-9, MMP-2, TGF-beta1 and tryptase, but not with TIMP-1. Significant correlations were noted between tryptase, and MMP-2, MMP-9, and TGF-beta1, but not with TIMP-1. Close correlations were noted between TGF-beta1, and MMP-9 and MMP-2, but not with TIMP-1. MMP-2, MMP-9, and TGF-beta1 may contribute to eosinophil and mast cell migrations into nasal polyp tissue.

Convergence of two major pathophysiologic mechanisms in nasal polyposis: Immune response to Staphylococcus aureus and airway remodeling

“…This imbalance can be partially explained by the lack of TGF-ß1 in NP and its inhibitory effect on MMP-9 activity via TIMP-1 release [13]. …”

Serum TGF-β1 as a Biomarker for Type 2 Diabetic Nephropathy: A Meta-Analysis of Randomized Controlled Trials

“…Generally, TGF-β family proteins are essential for regulating cellular growth, differentiation, autophagy, and apoptosis, as well as immune suppression [ 8 , 9 ]. However, TGF-β1 has also been recognized as a key mediator in ECM formation [ 10 ]. Up-regulation of TGF-β1 expression is reported to be indispensable in fibrosis and in tissue remodeling in various organs during disease progression [ 11 ], including glomerular fibrosis in the kidney [ 12 ].…”

Association of Inflammation Mediator in Mucosal and Tissue of Chronic Rhinosinusitis with Recurrent Nasal Polyp

“…Transforming growth factor-β1 (TGF-β1) is a chemoattractant for fibroblasts, stimulating fibroblast proliferation, and enhancing collagen laydown by fibroblasts. Of the TGF-isoforms, TGF-β1 synthesised by infiltrating eosinophils may contribute to stromal fibrosis and basement membrane thickening, which are characteristic of nasal polyp [25]. Transforming Growth Factor Beta1 plays an important role in the balance of fibrinolysis and fibrogenesis, which means it affects the extracellular matrix.…”