Brain-gut axis in the pathogenesis of Helicobacter pylori infection.
Helicobacter pylori (H. pylori) infection is the main pathogenic factor for upper digestive tract organic diseases. In addition to direct cytotoxic and proinflammatory effects, H. pylori infection may also induce abnormalities indirectly by affecting the brain-gut axis, similar to other microorganisms present in the alimentary tract. The brain-gut axis integrates the central, peripheral, enteric and autonomic nervous systems, as well as the endocrine and immunological systems, with gastrointestinal functions and environmental stimuli, including gastric and intestinal microbiota. The bidirectional relationship between H. pylori infection and the brain-gut axis influences both the contagion process and the host's neuroendocrine-immunological reaction to it, resulting in alterations in cognitive functions, food intake and appetite, immunological response, and modification of symptom sensitivity thresholds. Furthermore, disturbances in the upper and lower digestive tract permeability, motility and secretion can occur, mainly as a form of irritable bowel syndrome. Many of these abnormalities disappear following H. pylori eradication. H. pylori may have direct neurotoxic effects that lead to alteration of the brain-gut axis through the activation of neurogenic inflammatory processes, or by microelement deficiency secondary to functional and morphological changes in the digestive tract. In digestive tissue, H. pylori can alter signaling in the brain-gut axis by mast cells, the main brain-gut axis effector, as H. pylori infection is associated with decreased mast cell infiltration in the digestive tract. Nevertheless, unequivocal data concerning the direct and immediate effect of H. pylori infection on the brain-gut axis are still lacking. Therefore, further studies evaluating the clinical importance of these host-bacteria interactions will improve our understanding of H. pylori infection pathophysiology and suggest new therapeutic approaches.
Jacek Budzyński, Department of Gastroenterology, Vascular Diseases and Internal Medicine, Nicolaus Copernicus University, The Ludwik Rydygier Collegium Medicum in Bydgoszcz, 85-168 Bydgoszcz, Poland.
Jacek
J
Budzyński
Jacek Budzyński, Department of Gastroenterology, Vascular Diseases and Internal Medicine, Nicolaus Copernicus University, The Ludwik Rydygier Collegium Medicum in Bydgoszcz, 85-168 Bydgoszcz, Poland.
Maria
M
Kłopocka
D000208:Acute Disease; D000818:Animals; D001069:Appetite Regulation; D001835:Body Weight; D001921:Brain / Q000276:immunology / Q000503:physiopathology*; D002908:Chronic Disease; D003071:Cognition; D017615:Enteric Nervous System / Q000276:immunology / Q000382:microbiology* / Q000503:physiopathology*; D005247:Feeding Behavior; D005769:Gastrointestinal Motility; D041981:Gastrointestinal Tract / Q000276:immunology / Q000294:innervation* / Q000382:microbiology*; D016481:Helicobacter Infections / Q000276:immunology / Q000382:microbiology* / Q000503:physiopathology* / Q000523:psychology; D016480:Helicobacter pylori / Q000276:immunology / Q000472:pathogenicity*; D054884:Host-Pathogen Interactions; D006801:Humans; D008407:Mast Cells / Q000382:microbiology; D009435:Synaptic Transmission
Behavior; Brain-gut axis; Gastric acid; Helicobacter pylori; Motility; Visceral hypersensitivity