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.
Keywords
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Article info
Publication history
Published online: July 26, 2020
Accepted:
July 7,
2020
Received:
March 22,
2020
Identification
Copyright
© 2020 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
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- A further step forward in our knowledge of the pathogenetic role of gastroesophageal reflux in pulmonary fibrosisDigestive and Liver DiseaseVol. 52Issue 9
- PreviewPulmonary 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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