Persistent intestinal neuromuscular dysfunction after acute nematode infection in mice.

Although most acute enteric infections in humans resolve, some herald the onset of chronic symptomatology and persistent gastrointestinal dysfunction--so-called postinfectious irritable bowel syndrome. This entity is poorly understood, and there are no animal models for testing hypotheses. The aim of this study was to investigate changes in intestinal neuromuscular function during and after recovery from acute intestinal inflammation due to primary Trichinella spiralis infections in NIH Swiss mice. Morphometric scores and myeloperoxidase activity were used to monitor mucosal inflammation. Neuromuscular function was assessed in vitro by pharmacological or electrical stimulation of longitudinal muscle. Acute inflammation resulted in an approximately 50% reduction of villus height, an approximately 50% increase in crypt depth, and a threefold increase in myeloperoxidase activity. Carbachol- and KCl-induced contractions of longitudinal muscle were also increased threefold, whereas contraction induced by electrical field stimulation of intramural nerves was decreased by 60%. Mucosal morphology and myeloperoxidase activity rapidly returned to control values, but the increased muscle contractility and the decreased excitatory neurotransmission persisted as long as 42 and 28 days after infection, respectively. These findings show that transient mucosal inflammation alters enteric neuromuscular function; this alteration persists after recovery from the infection and mucosal restitution.