Effects of bacteria on the enteric nervous system: implications for the irritable bowel syndrome

Abstract

A unified scenario emerges when it is considered that a major impact of stress on the intestinal tract is reflected by symptoms reminiscent of the diarrhea-predominant form of irritable bowel syndrome. Cramping abdominal pain, fecal urgency, and explosive watery diarrhea are hallmarks not only of diarrhea-predominant irritable bowel syndrome, but also of infectious enteritis, radiation-induced enteritis, and food allergy. The scenario starts with stress-induced compromise of the intestinal mucosal barrier and continues with microorganisms or other sensitizing agents crossing the barrier and being intercepted by enteric mast cells. Mast cells signal the presence of the agent to the enteric nervous system (ie, the brain-in-the-gut), which uses one of the specialized programs from its library of programs to remove the "threat." This is accomplished by stimulating mucosal secretion, which flushes the threatening agent into the lumen and maintains it in suspension. The secretory response then becomes linked to powerful propulsive motility, which propels the secretions together with the offending agent rapidly in the anal direction. Cramping abdominal pain accompanies the strong propulsive contractions. Urgency is experienced when arrival of the large bolus of liquid distends the recto-sigmoid region and reflexly opens the internal anal sphincter, with continence protection now provided only by central reflexes that contract the puborectalis and external anal sphincter muscles. Sensory information arriving in the brain from receptors in the rapidly distending recto-sigmoid accounts for the conscious sensation of urgency and might exacerbate the individual's emotional stress. The symptom of explosive watery diarrhea becomes self-explanatory in this scenario.