Expression of transforming growth factor beta1 in bronchial biopsies in asthma and COPD.
ABSTRACT The role of transforming growth factor beta1 (TGF beta1) in airway remodeling in asthma and chronic obstructive pulmonary disease (COPD) has not been fully described. To evaluate the possible pathogenetic role of TGF beta1 in asthma and COPD, immunohistochemical expression of TGF beta1 was described in bronchial biopsies from patients with asthma and COPD compared with healthy individuals. Twelve subjects with asthma, 13 subjects with COPD, and 10 healthy individuals enrolled in the study. Bronchial biopsies were stained with hematoxylin and eosin and anti-TGF beta1 antibody. As a result, immunoreactive TGF beta1 was mainly localized in association with connective tissue in all groups. The staining intensity was not statistically different among the groups in bronchial epithelium, whereas it was significantly higher in the group of asthma in the submucosa. Because there is evidence showing a significant increase of staining intensity in the submucosa from asthmatics but not from subjects with COPD, we may conclude that TGF beta1 may play a significant role in pathogenesis of asthma but not in COPD.
- SourceAvailable from: Anna-Karin Larsson-Callerfelt[show abstract] [hide abstract]
ABSTRACT: Prostacyclin analogs are potent vasodilators and possess anti-inflammatory properties. However, the effect of prostacyclin on extracellular matrix (ECM) in COPD is not well known. Collagen fibrils and proteoglycans are essential ECM components in the lung and fibroblasts are key players in regulating the homeostasis of ECM proteins. The aim was to study the synthesis of prostacyclin and its effect on fibroblast activity and ECM production, and in particular collagen I and the collagen-associated proteoglycans biglycan and decorin. Parenchymal lung fibroblasts were isolated from lungs from COPD patients (GOLD stage IV) and from lungs and transbronchial biopsies from control subjects. The prostacyclin analog iloprost was used to study the effect of prostacyclin on ECM protein synthesis, migration, proliferation and contractile capacity of fibroblasts. TGF-β1 stimulation significantly increased prostacyclin synthesis in fibroblasts from COPD patients (p < 0.01), but showed no effect on fibroblasts from control subjects. Collagen I synthesis was decreased by iloprost in both control and COPD fibroblasts (p < 0.05). Conversely, iloprost significantly altered biglycan and decorin synthesis in control fibroblasts, but iloprost displayed no effect on these proteoglycans in COPD fibroblasts. Proliferation rate was reduced (p < 0.05) and contractile capacity was increased in COPD fibroblasts (p < 0.05) compared to control fibroblasts. Iloprost decreased proliferative rate in control fibroblasts (p < 0.05), whereas iloprost attenuated contraction capacity in both COPD (p < 0.01) and control fibroblasts (p < 0.05). Iloprost reduced collagen I synthesis and fibroblast contractility but did not affect the collagen-associated proteoglycans or proliferation rate in fibroblasts from COPD patients. Enhanced prostacyclin production could lead to improper collagen network fibrillogenesis and a more emphysematous lung structure in severe COPD patients.Respiratory research 01/2013; 14:21. · 3.64 Impact Factor
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ABSTRACT: Cytokines are small, secreted proteins that control immune responses. Within the lung, they can control host responses to injuries or infection, resulting in clearance of the insult, repair of lung tissue, and return to homeostasis. Problems can arise when this response is over exuberant and/or cytokine production becomes dysregulated. In such cases, chronic and repeated inflammatory reactions and cytokine production can be established, leading to airway remodeling and fibrosis with unintended, maladaptive consequences. In this report, we describe the cytokines and molecular mechanisms behind the pathology observed in three major chronic diseases of the lung: asthma, chronic obstructive pulmonary disease (COPD), and pulmonary fibrosis. Overlapping mechanisms are presented as potential sites for therapeutic intervention.F1000 Biology Reports 01/2013; 5:3.
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ABSTRACT: CD4+CD25+CD134+ T cells play an important role in suppressing T cell responses to foreign pathogens, including human immunodeficiency virus (HIV). Thus, we aimed to investigate an increase in these populations in HIV-1-infected individuals. In this study, we used a panel of monoclonal antibodies staining of CD3/CD4/CD25/CD134. Without antigen stimulation, the expression of CD4+CD25+CD134+ T cells in 14 HIV-1-infected and 24 healthy individuals were 4.01% and 3.21%, respectively. However, there was an increase in the expression of CD4 + CD25+CD134+ T cells in HIV-1-infected individuals (6.85%) when stimulated with gag peptide. The upregulation of CD4+CD25+CD134+ T cells in HIV-1-infected individuals may result from activation of naturally occurring or by disease-associated antigen stimulation.Journal of Immunoassay and Immunochemistry 04/2012; 33(2):195-202. · 0.73 Impact Factor