Helicobacter pylori, mucosal inflammation and symptom perception – new insights into an old hypothesis

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Abstract
The role of Helicobacter pylori and the accompanying mucosal inflammatory response in functional dyspepsia is still undefined. Human and animal studies have clearly demonstrated a link between intestinal mucosal inflammation and changes in sensory‐motor function. Growing clinical and basic evidence supports the concept that a similar paradigm may occur in H. pylori‐related dyspepsia. The infection may both induce gastric dysmotility and trigger neuroplastic changes in the afferent neural pathways leading to visceral hyperalgesia. A reduction of central antinociceptive control systems may also play a pathophysiological role. H. pylori eradication has provided disappointing results in terms of improvement of symptoms. This may reflect the long‐term recovery of neuroplastic changes occurring in the afferent nervous system or, alternatively, the incomplete resolution of gastritis and the persistent production of inflammatory mediators by resident cells in the muscularis externa.The identification of these mechanisms may provide a better understanding of the pathophysiology of H. pylori‐related dyspepsia and prompt innovative therapeutic approaches.