Abstract
Gastro-Oesophageal Reflux (GOR) has been associated with chronic airway diseases while the passage of foreign matter into airways and lungs through aspiration has the potential to initiate a wide spectrum of pulmonary disorders. The clinical syndrome resulting from such aspiration will depend both on the quantity and nature of the aspirate as well as the individual host response. Aspiration of gastric fluids may cause damage to airway epithelium, not only because acidity is toxic to bronchial epithelial cells but also due to the effect of digestive enzymes such as pepsin and bile salts. Experimental models have shown that direct instillation of these factors to airways epithelia cause damage with a consequential inflammatory response. The pathophysiology of these responses is gradually being dissected, with better understanding of acute gastric aspiration injury, a major cause of acute lung injury, providing opportunities for therapeutic intervention and potentially, ultimately, improved understanding of the chronic airway response to aspiration. Ultimately, clarification of the inflammatory pathways which are related to micro-aspiration via pepsin and bile acid salts may eventually progress to pharmacological intervention and surgical studies to assess the clinical benefits of such therapies in driving symptom improvement or reducing disease progression.
Highlights
Gastro-Oesophageal Reflux Disease (GORD) affects approximately 20% of the population of the western world [1]
Gastro-oesophageal reflux is caused by stomach contents leaking into the oesophagus, which in turn has the potential to lead to aspiration of these contents into the adjoining respiratory tract
IL-10 levels were the single best predictor of lung injury severity [40]. This finding is consistent with the interpretation that increases in this anti-inflammatory cytokine are important in protective responses against acute inflammation
Summary
Gastro-Oesophageal Reflux Disease (GORD) affects approximately 20% of the population of the western world [1]. In vivo and in vitro models have examined the effect of In those individuals who aspirate, recurrent respiratory tract infections are a common consequence, with the ensuing development of bronchiectasis a possible end-stage manifestation. The authors subsequently observed a significant reduction in LPS-induced cytokine production following weakly acidic shock treatment and subsequent prolonged exposure to endotoxin at normal pH, in turn potentially compromising the response to infection through the reduction in cytokine production and the potential for subsequent diminished immune cell recruitment. Recent research has shown that microbiological growth from gastric juice occurred when gastric juice pH was >4 and that the gastric and airway microbiome compositions of people with CF who reflux are similar in profile This novel data suggests the existence of an aero-digestive microbiome in CF, which may have clinical relevance. This host response to aspiration as well as its potential to induce changes in the pulmonary microbiome needs further investigation, with its importance only gradually gaining widespread recognition [12 - 14]
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