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E-JJRD-1

ABSTRACT: Transcription profiling of nodose or dorsal root ganglion visceral sensory neurons from mice infected with N. brasiliensis and/or subjected to environmental stress

TISSUE(S): Dorsal Root Ganglion Visceral Sensory Neurons, Nodose Ganglion Visceral Sensory Neurons

PROVIDER: E-JJRD-1 | ExpressionAtlas | 2015-10-22

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-JJRD-1-analysis-methods.tsv	Tabular
	E-JJRD-1-atlasExperimentSummary.Rdata	Rdata
	E-JJRD-1-configuration.xml	Xml
	E-JJRD-1-percentile-ranks.tsv	Tabular
	E-JJRD-1.condensed-sdrf.tsv	Tabular

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Transcription profiling of nodose or dorsal root ganglion visceral sensory neurons from mice infected with N. brasiliensis and/or subjected to environmental stress to determine molecular signatures for post-infective visceral chemosensitivity associated with irritable bowel syndrome

Project description:Background & Aims: Visceral hypersensitivity, a hallmark of irritable bowel syndrome, is generally considered to be mechanosensitive in nature and mediated via spinal afferents. Both stress and inflammation are implicated in visceral hypersensitivity, but the underlying molecular mechanisms of visceral hypersensitivity are unknown. <br> Methods: Mice were infected with Nippostrongylus brasiliensis (Nb) larvae, exposed to environmental stress and the following separate studies performed 3-4 weeks later. Mesenteric afferent nerve activity was recorded in response to either ramp balloon distension (60 mmHg), or to an intraluminal perfusion of hydrochloric acid (50 mM), or to octreotide administration (2 µM). Intraperitoneal injection of cholera toxin B-488 identified neurons projecting to the abdominal viscera. Fluorescent neurons in dorsal root and nodose ganglia were isolated using laser-capture microdissection. RNA was hybridised to Affymetrix Mouse whole genome arrays for analysis to evaluate the effects of stress and infection. <br> Results: In mice previously infected with Nb, there was no change in intestinal afferent mechanosensitivity, but there was an increase in chemosensitive responses to intraluminal hydrochloric acid when compared to control animals. Gene expression profiles in vagal but not spinal visceral sensory neurons were significantly altered in stressed Nb-infected mice. Decreased afferent responses to somatostatin receptor 2 stimulation correlated with lower expression of vagal somatostatin receptor 2 in stressed Nb-infected mice, confirming a link between molecular data and functional sequelae. <br> Conclusions: Alterations in the intestinal brain-gut axis, in chemosensitivity but not mechanosensitivity, and through vagal rather than spinal pathways, are implicated in stress-induced post-inflammatory visceral hypersensitivity.

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