Inflammation and Its Pathophysiological Role in Functional Dyspepsia

Abstract

Many individuals worldwide suffer from functional dyspepsia (FD), a chronic digestive disorder characterized by symptoms in the absence of observable structural abnormalities within the gastrointestinal system. This condition significantly impacts the quality of life and healthcare expenditures. Although the precise etiology of FD remains incompletely understood, recent research indicates that low-grade inflammation, particularly within the duodenum, constitutes a substantial component of its pathophysiology. Such inflammation involves immune system dysregulation, activation of mast cells and eosinophils, and the secretion of pro-inflammatory cytokines, which collectively contribute to duodenal inflammation. This inflammatory response disrupts the enteric nervous system and elevates visceral hypersensitivity. Hypersensitivity and diminished gastric motility are associated with dysbiosis of the gut microbiota and Helicobacter pylori infection, and these associations are mediated via the gut-brain axis. Increasing evidence suggests that alterations in the duodenal microbiota may underlie immunological irregularities and FD. Recent therapeutic approaches, including probiotics, antihistamines, and leukotriene inhibitors, have demonstrated promise in addressing the inflammatory pathways implicated in FD. The purpose of this review is to examine current evidence concerning the role of inflammation in the pathogenesis of FD and to consider its potential implications for the development of novel therapeutic strategies. A deeper understanding of these underlying processes may facilitate the development of effective, targeted treatments, thereby improving patient outcomes.