RESUMO
Gut commensals modulate host immune, endocrine, and metabolic functions. They also affect peripheral and central neural reflexes and function. We have previously shown that daily ingestion of Lactobacillus reuteri (LR) for 9 d inhibits the pseudoaffective cardiac response and spinal single-fiber discharge evoked by visceral distension, and decreases intestinal motility and myenteric AH cell slow afterhyperpolarization (sAHP) by inhibiting a Ca-activated K (IK(Ca)) channel. We tested whether luminal LR could acutely decrease motility in an ex vivo perfusion model of naive Balb/c jejunum. Live LR dose dependently decreased motor complex pressure wave amplitudes with 9- to 16-min onset latency and an IC(50) of 5 × 10(7) cells/ml Krebs. Heat-killed LR or another live commensal, Lactobacillus salivarius, were without effect. The IK(Ca) channel blocker TRAM-34, but neither the opener (DCEBIO) nor the hyperpolarization-activated cationic channel inhibitor ZD7288 (5 µM) (or TTX 1 µM), mimicked the LR effect on motility acutely ex vivo. We provide evidence for a rapid, strain-specific, dose-dependent action of a live Lactobacillus on small intestinal motility reflexes that recapitulates the long-term effects of LR ingestion. These observations may be useful as a first step to unraveling the pathways involved in bacteria to the nervous system communication.