P. Bercik

The anxiolytic effect of Bifidobacterium longum NCC3001 involves vagal pathways for gut–brain communication

Background  The probiotic Bifidobacterium longum NCC3001 normalizes anxiety‐like behavior and hippocampal brain derived neurotrophic factor (BDNF) in mice with infectious colitis. Using a model of chemical colitis we test whether the anxiolytic effect of B. longum involves vagal integrity, and changes in neural cell function.

Microbes and the gut-brain axis

Background  The ‘gut‐brain’ or ‘brain‐gut axis’, depending on whether we emphasize bottom‐up or top‐bottom pathways, is a bi‐directional communication system, comprised of neural pathways, such as the enteric nervous system (ENS), vagus, sympathetic and spinal nerves, and humoral pathways, which include cytokines, hormones, and neuropeptides as signaling molecules. Recent evidence, mainly arising from animal models, supports a role of microbes as signaling components in the gut‐brain axis.

Altered colonic function and microbiota profile in a mouse model of chronic depression

Depression often coexists with the irritable bowel syndrome (IBS) which is characterized by alterations in gut function. There is emerging evidence that the microbial composition (microbiota) of the gut is altered in IBS, but the basis for this is poorly understood. The aim of this study was to determine whether the induction of chronic depression results in changes in the colonic function and in its microbial community, and to explore underlying mechanisms.

The putative role of the intestinal microbiota in the irritable bowel syndrome

The irritable bowel syndrome (IBS) is a chronic abdominal symptom complex that is heterogeneous in terms of its clinical presentation and underlying pathophysiology and pathogenesis. It is now established that enteric infection can trigger the syndrome in at least a subset of patients. In addition, there is growing evidence of low grade inflammation and immune activation in the distal bowel of some IBS patients. These observations now prompt the question as to what maintains gut dysfunction in these patients. The intestinal microbiota influences a broad array of host organs that include the gut and the brain, and is an important determinant of normal function in these systems. Disruption of the delicate balance between the host and its intestinal microbiota (termed dysbiosis) results in changes in the mucosal immune system that range from overt inflammation as seen in Crohns Disease, to low grade inflammation without tissue injury, as seen in a subset of IBS patients. Under experimental conditions, disruption of the microbiota also produces changes in gut sensory-motor function and immune activity. Thus, dysbiosis induced by infection, dietary change or drugs such as antibiotics could produce low grade inflammation and chronic gut dysfunction, reminiscent of that seen in IBS. Fluctuations in gut physiology destabilize the habitat of commensal bacteria and provide a basis for chronic dysbiosis. Recent observations in animal models that changes in gut flora influence behavior provide a basis for a novel unifying hypothesis that accommodates both gut dysfunction and behavioral changes that characterize many IBS patients. This hypothesis states that dysbiosis exists in at least a subset of IBS patients, as a result of infection, dietary change or drugs and contributes to gut inflammatory and functional change in addition to psychiatric co-morbidity.

Oral administration of antigens from intestinal flora anaerobic bacteria reduces the severity of experimental acute colitis in BALB/c mice

Homeostasis between indigenous intestinal flora and host response may be broken in inflammatory bowel disease. The present study explores whether repeated oral administration of intestinal flora antigens can protect mice against dextran sodium sulphate (DSS)‐induced colitis. Sonicates of Gram‐positive, Gram‐negative, or anaerobic resident bacteria isolated from mouse intestinal flora were fed to BALB/c mice by gastric gavage, with or without cholera toxin. After four weekly doses of 1 mg of these antigen preparations (or of PBS as control), DSS colitis was induced. One week later colitis was evaluated by clinical scores and histology. Mice fed a pool of the three sonicates had decreased inflammation scores (5 (1–14); median (range)) compared with PBS‐fed control animals (15 (7–19); P < 0·05). Decreased inflammation was observed in mice fed anaerobic bacteria antigens (7 (6–11); P < 0·05 versus control), but not in mice fed a pool of Gram‐positive and ‐negative sonicates (16 (12–16)). Inflammation scores of mice fed antigens with cholera toxin were similar to those of PBS‐fed control animals. DSS‐induced colitis can be suppressed by oral administration of normal intestinal flora antigens containing anaerobes.

Transplantation of fecal microbiota from patients with irritable bowel syndrome alters gut function and behavior in recipient mice

Fecal microbiota transplants from patients with irritable bowel syndrome and anxiety alter gut function and behavior in germ-free mice. Connecting the gut-brain axis Irritable bowel syndrome (IBS), the most common gastrointestinal disorder worldwide, is characterized by abdominal pain and altered gut function and often is accompanied by anxiety. An association between intestinal dysbiosis and IBS has been reported, but the functional relevance remains unknown. De Palma and colleagues colonized germ-free mice with fecal microbiota from healthy controls or IBS patients with diarrhea (IBS-D) who did or did not have anxiety. They demonstrated that transplantation of fecal microbiota from patients with IBS-D and anxiety resulted in altered gut function and behavior in mouse recipients, including faster gastrointestinal transit, low-grade inflammation, and anxiety-like behavior. Irritable bowel syndrome (IBS) is a common disorder characterized by altered gut function and often is accompanied by comorbid anxiety. Although changes in the gut microbiota have been documented, their relevance to the clinical expression of IBS is unknown. To evaluate a functional role for commensal gut bacteria in IBS, we colonized germ-free mice with the fecal microbiota from healthy control individuals or IBS patients with diarrhea (IBS-D), with or without anxiety, and monitored gut function and behavior in the transplanted mice. Microbiota profiles in recipient mice clustered according to the microbiota profiles of the human donors. Mice receiving the IBS-D fecal microbiota showed a taxonomically similar microbial composition to that of mice receiving the healthy control fecal microbiota. However, IBS-D mice showed different serum metabolomic profiles. Mice receiving the IBS-D fecal microbiota, but not the healthy control fecal microbiota, exhibited faster gastrointestinal transit, intestinal barrier dysfunction, innate immune activation, and anxiety-like behavior. These results indicate the potential of the gut microbiota to contribute to both intestinal and behavioral manifestations of IBS-D and suggest the potential value of microbiota-directed therapies in IBS patients.

The effect of ammonia on omeprazole-induced reduction of gastric acidity in subjects with Helicobacter pylori infection.

The effect of ammonia on omeprazole-induced reduction of gastric acidity in subjects with Helicobacter pylori infection

No increase in prevalence of somatization in functional vs organic dyspepsia: a cross-sectional survey.

Psychological factors are associated with functional gastrointestinal (GI) disorders. Literature suggests that somatization is associated with functional dyspepsia (FD). However, the relationship between organic dyspepsia (OD), FD, and FD subtypes and somatization is poorly described. We aimed to examine this issue in a cross‐sectional study of secondary care patients.

Tracking gastrointestinal transit of solids in aged rats as pharmacological models of chronic dysmotility

Dysmotility in the gastrointestinal (GI) tract often leads to impaired transit of luminal contents leading to symptoms of diarrhea or constipation. The aim of this research was to develop a technique using high resolution X‐ray imaging to study pharmacologically induced aged rat models of chronic GI dysmotility that mimic accelerated transit (diarrhea) or constipation. The 5‐hydroxytryptamine type 4 (5‐HT4) receptor agonist prucalopride was used to accelerate transit, and the opioid agonist loperamide was used to delay transit.

Derivation and validation of a diagnostic test for irritable bowel syndrome using latent class analysis

The accuracy of symptom‐based diagnostic criteria for irritable bowel syndrome (IBS) is modest.