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Verdu EF, Bercik P, Verma-Gandhu M, et al. Specific probiotic therapy attenuates antibiotic induced visceral hypersensitivity in mice

Intestinal Disease Research Program, McMaster University, 1200 Main S West, Hamilton, Ontario, Canada.
Gut (Impact Factor: 14.66). 03/2006; 55(2):182-90. DOI: 10.1136/gut.2005.066100
Source: PubMed

ABSTRACT

Abdominal pain and discomfort are common symptoms in functional disorders and are attributed to visceral hypersensitivity. These symptoms fluctuate over time but the basis for this is unknown. Here we examine the impact of changes in gut flora and gut inflammatory cell activity on visceral sensitivity.
Visceral sensitivity to colorectal distension (CRD) was assessed at intervals in healthy mice for up to 12 weeks, and in mice before and after administration of dexamethasone or non-absorbable antibiotics with or without supplementation with Lactobacillus paracasei (NCC2461). Tissue was obtained for measurement of myeloperoxidase activity (MPO), histology, microbiota analysis, and substance P (SP) immunolabelling.
Visceral hypersensitivity developed over time in healthy mice maintained without sterile precautions. This was accompanied by a small increase in MPO activity. Dexamethasone treatment normalised MPO and CRD responses. Antibiotic treatment perturbed gut flora, increased MPO and SP immunoreactivity in the colon, and produced visceral hypersensitivity. Administration of Lactobacillus paracasei in spent culture medium normalised visceral sensitivity and SP immunolabelling, but not intestinal microbiota counts.
Perturbations in gut flora and in inflammatory cell activity alter sensory neurotransmitter content in the colon, and result in altered visceral perception. Changes in gut flora may be a basis for the variability of abdominal symptoms observed in functional gastrointestinal disorders and may be prevented by specific probiotic administration.

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    • "Since DSM decreased the firing frequency of nociceptive fibres, we wondered if the TRPV1 channel was involved since this is a major receptor involved in visceral nociception (Btesh et al.,2013). Verdu et al showed that antibiotic therapy induced visceral pain hypersensitivity which was inhibited by probiotic therapy (Verdu et al., 2006). Early life treatment of rats with vancomycin resulting in an altered gut microbiome, induced heightened visceral pain perception accompanied by a decrease in spinal cord TRPV1 expression (O'Mahony et al., 2014). "
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