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Alimentary Tract| Volume 52, ISSUE 9, P988-994, September 2020

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Stimulatory effect of gastroesophageal reflux disease (GERD) on pulmonary fibroblast differentiation

      Abstract

      Epidemiological studies indicate that prolonged micro-aspiration of gastric fluid is associated in gastroesophageal reflux disease with the development of chronic respiratory diseases, possibly caused by inflammation-related immunomodulation. Therefore, we sought to ascertain the effect of gastric fluid exposure on pulmonary residential cells. The expression of α-smooth muscle actin as a fibrotic marker was increased in both normal human pulmonary fibroblast cells and mouse macrophages. Gastric fluid enhanced the proliferation and migration of HFL-1 cells and stimulated the expression of inflammatory cytokines in an antibody assay. Elevated expression of the Rho signaling pathway was noted in fibroblast cells stimulated with gastric fluid or conditioned media. These results indicate that gastric fluid alone, or the mixture of proinflammatory mediators induced by gastric fluid in the pulmonary context, can stimulate pulmonary fibroblast cell inflammation, migration, and differentiation, suggesting that a wound healing process is initiated. Subsequent aberrant repair in pulmonary residential cells may lead to pulmonary fibroblast differentiation and fibrotic progression. The results point to a stimulatory effect of chronic GERD on pulmonary fibroblast differentiation, and this may promote the development of chronic pulmonary diseases in the long term.

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      Linked Article

      • A further step forward in our knowledge of the pathogenetic role of gastroesophageal reflux in pulmonary fibrosis
        Digestive and Liver DiseaseVol. 52Issue 9
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          Pulmonary fibrosis is a repair response in lung tissue injury that involves loss of epithelial cells and accumulation of fibroblasts/myofibroblasts [1]. The main triggers of this fibrotic progression might be viral infections, organic and inorganic dusts, smoking and Gastroesophageal Reflux Disease (GERD). Furthermore, the majority of published studies have suggested that there is a strong comorbidity between GERD and Idiopathic pulmonary fibrosis (IPF) [2,3]. Based on this knowledge, we have read with interest the paper entitled “Stimulatory Effect of Gastroesophageal Reflux Disease (GERD) on Pulmonary Fibroblast Differentiation” written by Cheng et al [4].
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