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Controversy surrounding the increased expression of TGF beta 1 in asthma.

ABSTRACT: Asthma is a waxing and waning disease that leads to structural changes in the airways, such as subepithelial fibrosis, increased mass of airway smooth muscle and epithelial metaplasia. Such a remodeling of the airways further amplifies asthma symptoms, but its etiology is unknown. Transforming growth factor beta1 is a pleiotropic cytokine involved in many fibrotic, oncologic and immunologic diseases and is believed to play an essential role in airway remodeling that occurs in asthmatic patients. Since it is secreted in an inactive form, the overall activity of this cytokine is not exclusively determined by its level of expression, but also by extensive and complex post-translational mechanisms, which are all important in modulating the magnitude of the TGFbeta1 response. Even if TGFbeta1 upregulation in asthma is considered as a dogma by certain investigators in the field, the overall picture of the published literature is not that clear and the cellular origin of this cytokine in the airways of asthmatics is still a contemporaneous debate. On the other hand, it is becoming clear that TGFbeta1 signaling is increased in the lungs of asthmatics, which testifies the increased activity of this cytokine in asthma pathogenesis. The current work is an impartial and exhaustive compilation of the reported papers regarding the expression of TGFbeta1 in human asthmatics. For the sake of comparison, several studies performed in animal models of the disease are also included. Inconsistencies observed in human studies are discussed and conclusions as well as trends from the current state of the litterature on the matter are proposed. Finally, the different points of regulation that can affect the amplitude of the TGFbeta1 response are briefly revised and the possibility that TGFbeta1 is dysregulated at another level in asthma, rather than simply in its expression, is highlighted.

SUBMITTER: Bosse Y

PROVIDER: S-EPMC2078588 | biostudies-literature | 2007 Sep

REPOSITORIES: biostudies-literature

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Controversy surrounding the increased expression of TGF beta 1 in asthma.

Bossé Ynuk Y Rola-Pleszczynski Marek M

Respiratory research 20070924

Asthma is a waxing and waning disease that leads to structural changes in the airways, such as subepithelial fibrosis, increased mass of airway smooth muscle and epithelial metaplasia. Such a remodeling of the airways further amplifies asthma symptoms, but its etiology is unknown. Transforming growth factor beta1 is a pleiotropic cytokine involved in many fibrotic, oncologic and immunologic diseases and is believed to play an essential role in airway remodeling that occurs in asthmatic patients. ...[more]

PMID: 17892594

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Project description:Recent studies have suggested that eosinophils may have a direct effect on airway smooth muscle cells (ASMC), causing their proliferation in patients with asthma, but the precise mechanism of the interaction between these cells remains unknown. We propose that changes in Wnt signaling activity and extracellular matrix (ECM) production may help explain these findings. Therefore, the aim of this study was to investigate the effect of eosinophils from asthmatic and non-asthmatic subjects on Wnt-5a, transforming growth factor ?1 (TGF-?1), and ECM protein (fibronectin and collagen) gene expression and ASMC proliferation.A total of 18 subjects were involved in the study: 8 steroid-free asthma patients and 10 healthy subjects. Peripheral blood eosinophils were isolated using centrifugation and magnetic separation. An individual co-culture of eosinophils with human ASMC was prepared for each study subject. Adhesion of eosinophils to ASMC (evaluated by assaying eosinophil peroxidase activity) was determined following various incubation periods (30, 45, 60, 120, and 240 min). The expression of Wnt-5a, TGF-?1, and ECM protein genes in ASMC was measured using quantitative real-time polymerase chain reaction (PCR) after 24 h of co-culture. Proliferation of ASMC was measured using the Alamar blue method after 48 h and 72 h of co-culture with eosinophils.Eosinophils from asthmatic subjects demonstrated increased adhesion to ASMC compared with eosinophils from healthy subjects (p?<?0.05) in vitro. The expression of Wnt-5a, TGF-?1, collagen, and fibronectin genes in ASMC was significantly higher after 24 h of co-culture with eosinophils from asthmatic subjects, while co-culture of ASMC with eosinophils from healthy subjects increased only TGF-?1 and fibronectin gene expression. ASMC proliferation was augmented after co-culture with eosinophils from asthma patients compared with co-culture with eosinophils from healthy subjects (p?<?0.05).Eosinophils enhance Wnt-5a, TGF-?1, fibronectin, and collagen gene expression in ASMC and promote proliferation of these cells in asthma.ClinicalTrials.gov Identifier: NCT02648074 .

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Controversy surrounding the increased expression of TGF beta 1 in asthma.

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Controversy surrounding the increased expression of TGF beta 1 in asthma.

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