Gastro-oesophageal reflux disease (GORD) is a chronic condition characterised by visceral pain in the distal oesophagus. The current first-line treatment for GORD is proton pump inhibitors (PPIs), however, PPIs are ineffective in a large cohort of patients and long-term use may have adverse effects. Emerging evidence suggests that nerve fibre number and location are likely to play interrelated roles in nociception in the oesophagus of GORD patients. Simultaneously, alterations in cells of the oesophageal mucosa, namely epithelial cells, mast cells, dendritic cells, and T lymphocytes, have been a focus of GORD research for several years. The oesophagus of GORD patients exhibits both macro- and micro-inflammation as a response to chronic acidic reflux at the epithelium. In other conditions of the GI tract, such as IBS and IBD, well-characterised bidirectional processes between immune cells and mucosal nerve fibres contribute to pathogenesis and symptom generation. Sensory alterations in these conditions such as nerve fibre outgrowth and hypersensitivity can be driven by inflammatory processes, which promote visceral pain signalling. This review will examine what is currently known of the molecular pathways linking inflammation and sensory perception leading to the development of GORD symptoms and explore potentially relevant mechanisms in other GI regions which may indicate new areas in GORD research.

胃食管反流病（GORD）是一种慢性疾病，其特征是远端食管内脏疼痛。目前 GORD 的一线治疗是质子泵抑制剂（PPI），但 PPI 对大量患者无效，长期使用可能会产生不良反应。新的证据表明，神经纤维的数量和位置可能在 GORD 患者食道的伤害感受中发挥相互关联的作用。同时，食管粘膜细胞（即上皮细胞、肥大细胞、树突状细胞和 T 淋巴细胞）的改变多年来一直是 GORD 研究的焦点。GORD 患者的食管表现出宏观和微观炎症，这是对上皮慢性酸性反流的反应。在胃肠道的其他病症中，例如IBS和IBD，免疫细胞和粘膜神经纤维之间特征明确的双向过程有助于发病机制和症状的产生。这些情况下的感觉改变，例如神经纤维生长和超敏反应，可能是由炎症过程驱动的，从而促进内脏疼痛信号传导。这篇综述将研究目前已知的连接炎症和感觉知觉导致 GORD 症状发展的分子途径，并探讨其他胃肠道区域的潜在相关机制，这可能表明 GORD 研究的新领域。