<i>Lactobacillus reuteri</i> ingestion prevents hyperexcitability of colonic DRG neurons induced by noxious stimuli

Ma, Xuelian; Mao, Yu; Wang, Bingxian; Huizinga, Jan D.; Bienenstock, John; Kunze, Wolfgang

doi:10.1152/ajpgi.90511.2008

Cited by 87 publications

(79 citation statements)

References 52 publications

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“…Lactobacillus rhamnosus (JB-1) was taken from in-house stock 4,7,12 . This bacterium was wrongly identified in several previous publications as L. reuteri and has now been confirmed as a L. rhamnosus by whole-genome sequence analysis.…”

Section: Methodsmentioning

confidence: 99%

“…Bacteria were heat-killed by heating to 80°C for 20 min after which they lost all viability as shown by cultures up to 72 h after plating. All other related methods are as reported previously 4,7,12 . Live JB-1 were grown from frozen ( À 80°C) 1 ml aliquots, which consisted of 9.7 log c.f.u.…”

Section: Methodsmentioning

confidence: 99%

“…Yet the effects on intrinsic enteric neurons are largely unexplored. Feeding with certain bacterial species and strains reduces the perception of visceral pain [3][4][5][6] , decreases activity in spinal single afferent fibres 4 and inhibits colorectal distension induced sensitization of dorsal root ganglion neurons 7 . Ingestion of a Lactobacillus rhamnosus strain, 'JB-1', (ref.…”

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confidence: 99%

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Bacteroides fragilis polysaccharide A is necessary and sufficient for acute activation of intestinal sensory neurons

et al. 2013

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Symbionts or probiotics are known to affect the nervous system. To understand the mechanisms involved, it is important to measure sensory neuron responses and identify molecules responsible for this interaction. Here we test the effects of adding Lactobacillus rhamnosus (JB-1) and Bacteroides fragilis to the epithelium while making voltage recordings from intestinal primary afferent neurons. Sensory responses are recorded within 8 s of applying JB-1 and excitability facilitated within 15 min. Bacteroides fragilis produces similar results, as does its isolated, capsular exopolysaccharide, polysaccharide A. Lipopolysaccharide-free polysaccharide A completely mimics the neuronal effects of the parent organism. Experiments with a mutant Bacteroides fragilis devoid of polysaccharide A shows that polysaccharide A is necessary and sufficient for the neuronal effects. Complex carbohydrates have not been reported before as candidates for such signalling between symbionts and the host. These observations indicate new neuronal targets and invite further study of bacterial carbohydrates as inter-kingdom signalling molecules between beneficial bacteria and sensory neurons.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Bacteroides fragilis polysaccharide A is necessary and sufficient for acute activation of intestinal sensory neurons

et al. 2013

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“…2,3,[40][41][42][43] In GF mice, contact with commensal microbiota is necessary for mice to develop pain sensitivity, possibly in a toll-like receptor (TLR)-dependent manner. 1 Inflammatory hyper nociception induced by diverse stimuli, including lipopolysaccharide (LPS) and Interleukin (IL)-1 is reduced in GF mice.…”

Section: Alterations In the M Icrobiome And Visceral Pain Responses Imentioning

confidence: 99%

Visceral Pain and Gastrointestinal Microbiome

Chichlowski

Rudolph

2015

J Neurogastroenterol Motil

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A complex set of interactions between the microbiome, gut and brain modulate responses to visceral pain. These interactions occur at the level of the gastrointestinal mucosa, and via local neural, endocrine or immune activity; as well as by the production of factors transported through the circulatory system, like bacterial metabolites or hormones. Various psychological, infectious and other stressors can disrupt this harmonious relationship and alter both the microbiome and visceral pain responses. There are critical sensitive periods that can impact visceral pain responses in adulthood. In this review we provide a brief background of the intestinal microbiome and emerging concepts of the bidirectional interactions between the microbiome, gut and brain. We also discuss recent work in animal models, and human clinical trials using prebiotics and probiotics that alter the microbiome with resultant alterations in visceral pain responses.

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“…One such organism is Lactobacillus rhamnosus (JB-1), which has been demonstrated to modulate the immune system because it prevents the induction of IL-8 by TNF-α in human colon epithelial cell lines (T84 and HT-29) (17) and modulates inflammation through the generation of regulatory T cells (18). Moreover, it inhibits the cardio-autonomic response to colorectal distension (CRD) in rats (19), reduces CRD-induced dorsal root ganglia excitability (20), and affects small intestine motility (21).…”

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Ingestion of Lactobacillus strain regulates emotional behavior and central GABA receptor expression in a mouse via the vagus nerve

Bravo¹,

Forsythe

Chew

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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There is increasing, but largely indirect, evidence pointing to an effect of commensal gut microbiota on the central nervous system (CNS). However, it is unknown whether lactic acid bacteria such as Lactobacillus rhamnosus could have a direct effect on neurotransmitter receptors in the CNS in normal, healthy animals. GABA is the main CNS inhibitory neurotransmitter and is significantly involved in regulating many physiological and psychological processes. Alterations in central GABA receptor expression are implicated in the pathogenesis of anxiety and depression, which are highly comorbid with functional bowel disorders. In this work, we show that chronic treatment with L. rhamnosus (JB-1) induced region-dependent alterations in GABA B1b mRNA in the brain with increases in cortical regions (cingulate and prelimbic) and concomitant reductions in expression in the hippocampus, amygdala, and locus coeruleus, in comparison with control-fed mice. In addition, L. rhamnosus (JB-1) reduced GABA Aα2 mRNA expression in the prefrontal cortex and amygdala, but increased GABA Aα2 in the hippocampus. Importantly, L. rhamnosus (JB-1) reduced stress-induced corticosterone and anxiety-and depression-related behavior. Moreover, the neurochemical and behavioral effects were not found in vagotomized mice, identifying the vagus as a major modulatory constitutive communication pathway between the bacteria exposed to the gut and the brain. Together, these findings highlight the important role of bacteria in the bidirectional communication of the gut-brain axis and suggest that certain organisms may prove to be useful therapeutic adjuncts in stressrelated disorders such as anxiety and depression.brain-gut axis | irritable bowel syndrome | probiotic | fear conditioning | cognition T here is increasing evidence suggesting an interaction between the intestinal microbiota, the gut, and the central nervous system (CNS) in what is recognized as the microbiome-gut-brain axis (1-4). Studies in rodents have implicated dysregulation of this axis in functional bowel disorders, including irritable bowel syndrome. Indeed, visceral perception in rodents can be affected by alterations in gut microbiota (5). Moreover, it has been shown that the absence and/or modification of the gut microflora in mice affects the hypothalamic-pituitary-adrenal (HPA) axis response to stress (6, 7) and anxiety behavior (8, 9), which is important given the high comorbidity between functional gastrointestinal disorders and stress-related psychiatric disorders, such as anxiety and depression (10). In addition, pathogenic bacteria in rodents can induce anxiety-like behaviors, which are mediated via vagal afferents (9, 11).GABA is the main inhibitory neurotransmitter of the CNS, the effects of which are mediated through two major classes of receptors-the ionotropic GABA A receptors, which exist as a number of subtypes formed by the coassembly of different subunits (α, β, and γ subunits; ref. 12), and the GABA B receptors, which are G protein coupled and consist of a heterodi...

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Lactobacillus reuteri ingestion prevents hyperexcitability of colonic DRG neurons induced by noxious stimuli

Cited by 87 publications

References 52 publications

Bacteroides fragilis polysaccharide A is necessary and sufficient for acute activation of intestinal sensory neurons

Bacteroides fragilis polysaccharide A is necessary and sufficient for acute activation of intestinal sensory neurons

Visceral Pain and Gastrointestinal Microbiome

Ingestion of Lactobacillus strain regulates emotional behavior and central GABA receptor expression in a mouse via the vagus nerve

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