Gastro-oesophageal reflux and idiopathic pulmonary fibrosis: sorting the chicken and the egg by genetic link

Idiopathic pulmonary fibrosis (IPF) is a devastating condition that confers substantial morbidity and significantly reduces lifespan. Because of this, investigators have searched for modifiable risk factors to reduce the burden of IPF. While the aetiological holy grail for IPF remains elusive, there is mounting evidence that prevalent lung injuries on a background of genetic susceptibility culminate in this rare and “idiopathic” disease. Gastro-oesophageal reflux may be one of these prevalent lung injuries that culminate in lung fibrosis. In preclinical models, gastric acid aspiration into the lungs can trigger an inflammatory response and induce expression of transforming growth factor-β, resulting in epithelial–mesenchymal transition and interstitial collagen deposition [1–4]. Genetic factors predispose for gastro-oesophageal reflux and idiopathic pulmonary fibrosis