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Introduction The lung, a vital organ for gas exchange in humans and most mammals, is prone to various respiratory disorders, including pulmonary fibrosis, pneumonia, and lung cancer, during the aging process (Selman et al., 2016; Selman et al., 2016). Pulmonary fibrosis arises from repetitive and widespread lung injury, in which normal healing process becomes dysregulated and functional tissue is replaced with fibrous scar tissue (Bochaton-Piallat et al., 2016).
Introduction Idiopathic pulmonary fibrosis (IPF) is a rare, chronic, progressive, fibrotic, interstitial lung disease with unknown etiology and pathogenesis (1). It mainly affects the middle-aged and elderly population with a poor prognosis. It is clinically characterized by progressive scarring or fibrosis of the interstitial lung, leading to a gradual decline in lung function and eventual death (2, 3).
Tumor necrosis factor-alpha (TNF-?) is a potent pro-inflammatory mediator and its expression is up-regulated in chronic obstructive pulmonary disease (COPD). Tristetraprolin (TTP) is implicated in regulation of TNF-? expression; however, whether TTP is involved in cigarette smoke-induced TNF-? expression has not been determined. TTP expression was examined by western blot analysis in murine alveolar macrophages and alveolar epithelial cells challenged without or with cigarette smoke extract (CSE).
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