Transforming Growth Factor-beta1 as Lung Injury Biomarker: a Review

Lung injury, induced by chemicals, radiotherapy or others agents is marked by enhancement in the expression of transforming growth factor beta1 (TGF-1) as a result of inflammation. TGF-1 appears to be the major profibrogenic cytokine which regulates the production and deposition of the major extracellular matrix molecules (ECM) and has been reported to be involved in a host of cellular responses. Therefore, it has been attempted in this review to evaluate the role of TGF-1 as a biomarker of lung injury, both at acute and late phase, in different models of lung injury. The up-regulation of TGF-1 mRNA expression and its corresponding protein in lung tissue subsequent to infliction of tissue injury has been established by various investigations involving RT-PCR analysis, Western blotting involving TGF-1 antibody, immunohistochemical and immunolocalisation studies, etc. Increase in the expression of TGF-1 at the acute phase triggers the tissue repair mechanisms involving the synthesis of ECM proteins and other cellular mediators of tissue repair, a hallmark of development and progression of fibrosis. Experimental evidences reviewed in this article indicate that TGF-1 is probably the main biomarker of lung injury induced by various agents and appears to contribute very significantly in the development of fibrosis. Additionally, experimental evidences also suggest that it may not act alone but rather by activation or in combination with other proinflammatory molecules in response to lung tissue injury.