Abstract: The pathogenesis of GERD symptoms may have a multifactorial mechanism, in which noxious factors, including acid-pepsin and acid, are involved. The interaction of relfuxed content and esophageal mucosa probably caused by a defective luminal clearance and mucosa barrier mechanisms, would be responsible for visual detectable lesion of esophageal mucosa. The researches of animal models with long time contact of acid content demonstrated that receptors on nerve endings may be involved in esophageal sensitivity and nociception. At the meantime, speciifc chemokine and cytokine may explain the different esophageal subtypes of GERD, partly illuminating the genesis of esophagitis in a subtype. Researches indicate that there are additional neurotransmitters and inlfammatory mediators in GERD patients, the relationship of the esophageal inlfammation and hypersensitivity is still not clear. Moreover, over 70%of GERD patients don’t to be erosive, a subset called non-erosive relfux disease. This summary aims to elucidate the pathogenesis of inlfammatory in GERD to differentiate erosive and non-erosive relfux disease and provide new therapeutic approaches.

Key words: gastroesophageal relfux disease, perception, mechanism, symptom, pathogenesis