Escherichia coli heat-stable toxin: its effect on motility of the small intestine

Abstract

Escherichia coli heat-stable enterotoxin is a low-molecular-weight substance that has been shown to induce the active secretion of fluid and electrolytes in the small intestine. In this study, we have characterized the effects of purified E. coli heat-stable toxin (ST, strain 18D, serotype 042:K86:H37) on the motility of rabbit small intestine by using myoelectric recording techniques. Substances, such as cholera toxin, that activate the adenylate cyclase-cAMP system induced predominantly migrating action-potential complex activity. E. coli ST, a toxin that activates the guanylate cyclase-cGMP system, was infused into isolated in vivo ileal loops of New Zealand White rabbits. Inactivated toxin was also studied by exposing the ST to 1 mM dithiothreitol for 90 min. Active E. coli ST induced only repetitive bursts of action potentials. When the toxin was inactivated with dithiothreitol, no alteration in myoelectric activity was observed. We speculate that repetitive bursts of action-potential activity may represent a virulent factor of the bacterium, altering motor activity to slow transit and allowing for bacterial proliferation and invasion.

The Enteric Nervous System and Its Extrinsic Connections

“…The intestine exhibits exaggerated secretomotor reflexes, causing diarrhea, when levels of bacteria and bacterial toxins in the gut lumen are excessive [184,185]. Bacteria and parasites in the gut lumen also trigger powerful propulsive reflexes that help to expel these organisms [186][187][188]. Vomiting, which involves retropulsive reflexes in the small intestine, is also used to eliminate undesirable contents from the gut.…”

Protective Effect of a Lipoxygenase Inhibitor, Nordihydroguaretic Acid, on the Ileal Motor Disturbances Induced by Serratia marcescens Endotoxin in Rats

“…There is much evidence that endotoxins play a significant role in endotoxemic shock and gastrointestinal motility disturbances. 6,13,[15][16][17][18][19][20][21] According to a number of experimental studies, the first effects of endotoxin were seen after 60 min and it seems likely that these effects were indirect. 15,22 The symptoms were most severe 90-120 min after endotoxin injection, 22 and endotoxin produced profound disruption of normal fasting bowel motility patterns.…”

“…17 Motility disturbances resulting from endotoxemia are still a major concern, and prostaglandins have been increasingly implicated as significant pathophysiologic mediators in circulatory shock. 1,6,12,16,17,22 The effect of LTs is similar to many of the pathophysiologic sequelae of endotoxemia. Several studies have suggested that LTs may be significant pathogenic mediators in endotoxemia.…”

NONRUMINANT NUTRITION SYMPOSIUM: Involvement of gut neural and endocrine systems in pathological disorders of the digestive tract1,2

“…The secretomotor reflex pathways that are stimulated by cholera toxin pass through the myenteric plexus, and the reflex is prevented by ablating this plexus (Jodal et al, 1993). Defensive responses, such as the reverse peristalsis in the small intestine that occurs in vomiting, and exaggerated propulsive activity (Mathias et al, 1982;Vallance et al, 1997) and secretion (Lundgren, 2002) in the large intestine are mediated through the enteric nervous system and can be triggered by noxious chemicals or pathogens.…”