title: The relationship between intestinal microbiota and the central nervous system in normal gastrointestinal function and disease.
abstract: Although many people are aware of the communication that occurs between the gastrointestinal (GI) tract and the central nervous system, fewer know about the ability of the central nervous system to influence the microbiota or of the microbiota's influence on the brain and behavior. Within the GI tract, the microbiota have a mutually beneficial relationship with their host that maintains normal mucosal immune function, epithelial barrier integrity, motility, and nutrient absorption. Disruption of this relationship alters GI function and disease susceptibility. Animal studies suggest that perturbations of behavior, such as stress, can change the composition of the microbiota; these changes are associated with increased vulnerability to inflammatory stimuli in the GI tract. The mechanisms that underlie these alterations are likely to involve stress-induced changes in GI physiology that alter the habitat of enteric bacteria. Furthermore, experimental perturbation of the microbiota can alter behavior, and the behavior of germ-free mice differs from that of colonized mice. Gaining a better understanding of the relationship between behavior and the microbiota could provide insight into the pathogenesis of functional and inflammatory bowel disorders.
authors.affiliation: The Farncombe Family Digestive Health Research Institute, Faculty of Health Sciences, McMaster University, Hamilton, Ontario, Canada. scollins@mcmaster.ca
authors.forename: Stephen M
authors.initials: SM
authors.lastname: Collins
authors.forename: Premsyl
authors.initials: P
authors.lastname: Bercik
mesh_terms: D000818:Animals; D002493:Central Nervous System Diseases / Q000150:complications* / Q000453:epidemiology; D005767:Gastrointestinal Diseases / Q000150:complications / Q000453:epidemiology / Q000382:microbiology*; D041981:Gastrointestinal Tract / Q000382:microbiology* / Q000502:physiology*; D014943:Global Health; D006801:Humans; D009017:Morbidity; D012307:Risk Factors