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World J Gastroenterol. May 14, 2014; 20(18): 5212-5225
Published online May 14, 2014. doi: 10.3748/wjg.v20.i18.5212
Brain-gut axis in the pathogenesis of Helicobacter pylori infection
Jacek Budzyński, Maria Kłopocka
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 Budzyński, Clinical Ward of Vascular Diseases and Internal Medicine, The Jan Biziel University Hospital No. 2, 85-168 Bydgoszcz, Poland
Maria Kłopocka, Department of Gastroenterological Nursing, Nicolaus Copernicus University, The Ludwik Rydygier Collegium Medicum in Bydgoszcz, 85-168 Bydgoszcz, Poland
Author contributions: Budzyński J conceived of and wrote the manuscript; Kłopocka M revised the manuscript; Budzyński J and Kłopocka M performed the literature review, wrote the paper and approved the final revised version.
Correspondence to: Jacek Budzyński, MD, PhD, Clinical Ward of Vascular Diseases and Internal Medicine, The Jan Biziel University Hospital No. 2, Ujejskiego 75 Street, 85-168 Bydgoszcz, Poland. budz@cps.pl
Telephone: +48-52-3655347 Fax: +48-52-3655347
Received: September 25, 2013
Revised: January 11, 2014
Accepted: January 19, 2014
Published online: May 14, 2014
Processing time: 231 Days and 5.4 Hours
Abstract

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.

Keywords: Helicobacter pylori; Brain-gut axis; Behavior; Motility; Gastric acid; Visceral hypersensitivity

Core tip: This manuscript is the first review concerning the interplay between Helicobacter pylori (H. pylori) infection and the brain-gut axis. Data from relevant publications, including both human and animal studies, were grouped and discussed according to the pathophysiological mechanisms of interactions between H. pylori and host reaction.