Plasticity of dorsal root ganglion neurons in a rat model of post-infectious gut dysfunction: potential implication of nerve growth factor

Jardí, Ferran; Fernández-Blanco, Joan Antoni; Martı́nez, Vicente; Vergara, P.

doi:10.3109/00365521.2014.958524

Cited by 13 publications

(15 citation statements)

References 32 publications

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“…45 Additionally, NGF has been implicated in the sensitization of visceral afferents, leading to the development of hypersensitivity. 46 Therefore, NGF downregulation might also contribute to the analgesic-like responses observed here.…”

Section: Discussionmentioning

confidence: 97%

Antibiotic-induced dysbiosis alters host-bacterial interactions and leads to colonic sensory and motor changes in mice

2015

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Abbreviations: AMP, antimicrobial peptide; CB1/2, cannabinoid receptor type 1 or 2; FGD, functional gastrointestinal disorder; FISH, fluorescent in situ hybridization; GCM, gut commensal microbiota; GI, gastrointestinal; IBS, irritable bowel syndrome; iNOS, inducible nitric oxide synthase; MOR, mu-opioid receptor; NGF, nerve growth factor; PPR, pattern recognition receptor; Reg3g, regenerating islet-derived protein 3 gamma; RELMb, resistin-like molecule-b; RT-qPCR, reverse transcription quantitative polymerase chain reaction; SFB, segmented filamentous bacteria; sIgA, secretory IgA; TLR, toll-like receptor; TPH 1/2, tryptophan hydroxylase isoforms 1 or 2; TRPV1/3, transient receptor potential vanilloid types 1 or 3Alterations in the composition of the commensal microbiota (dysbiosis) seem to be a pathogenic component of functional gastrointestinal disorders, mainly irritable bowel syndrome (IBS), and might participate in the secretomotor and sensory alterations observed in these patients.We determined if a state antibiotics-induced intestinal dysbiosis is able to modify colonic pain-related and motor responses and characterized the neuro-immune mechanisms implicated in mice. A 2-week antibiotics treatment induced a colonic dysbiosis (increments in Bacteroides spp, Clostridium coccoides and Lactobacillus spp and reduction in Bifidobacterium spp). Bacterial adherence was not affected. Dysbiosis was associated with increased levels of secretory-IgA, up-regulation of the antimicrobial lectin RegIIIg, and toll-like receptors (TLR) 4 and 7 and down-regulation of the antimicrobial-peptide Resistin-Like Molecule-b and TLR5. Dysbiotic mice showed less goblet cells, without changes in the thickness of the mucus layer. Neither macroscopical nor microscopical signs of inflammation were observed. In dysbiotic mice, expression of the cannabinoid receptor 2 was up-regulated, while the cannabinoid 1 and the mu-opioid receptors were down-regulated. In antibiotic-treated mice, visceral painrelated responses elicited by intraperitoneal acetic acid or intracolonic capsaicin were significantly attenuated. Colonic contractility was enhanced during dysbiosis. Intestinal dysbiosis induce changes in the innate intestinal immune system and modulate the expression of pain-related sensory systems, an effect associated with a reduction in visceral painrelated responses. Commensal microbiota modulates gut neuro-immune sensory systems, leading to functional changes, at least as it relates to viscerosensitivity. Similar mechanisms might explain the beneficial effects of antibiotics or certain probiotics in the treatment of IBS.

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Section: Discussionmentioning

confidence: 97%

Antibiotic-induced dysbiosis alters host-bacterial interactions and leads to colonic sensory and motor changes in mice

2015

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“…Thus, it is feasible to speculate that these differences might be either related to the degree of inflammation observed or, more interestingly, a compensatory response observed outside the primary inflammatory site. During T. spiralis infection, the primary site of inflammation is the jejunum, with the colon showing a comparatively attenuated inflammatory‐like response . Therefore, inflammation‐dependent modulation of NTFs might depend on the intensity of the inflammatory response elicited.…”

Section: Discussionmentioning

confidence: 99%

“…In this model, we assessed, up to 30 days PI, inflammatory‐like changes and mast cells (mucosal and connective type) dynamics in the colon, a site not directly affected during T. spiralis infection, which shows tropism for the small intestine and courses primarily with a jejunitis. Previously, we described a persistent hypertrophy of thoracolumbar (T10‐L2) dorsal root ganglia (DRG) neurons at chronic stages of T. spiralis infection, although the levels of NGF in the intestine were unaltered at 30 days PI . Therefore, here, to explore the potential implication of NTFs, we studied the evolution in time of the expression of NGF, GDNF, artemin, and neurturin and their receptors (TrkA and GFR α 3) in colonic tissues and in thoracolumbar (TL) and lumbosacral (LS) DRG neurons.…”

Section: Introductionmentioning

confidence: 99%

Persistent alterations in colonic afferent innervation in a rat model of postinfectious gut dysfunction: Role for changes in peripheral neurotrophic factors

Jardí

Fernández-Blanco

Martı́nez

et al. 2016

Neurogastroenterology Motil

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“…Extensive evidence suggests that NGF is an important pain mediator . NGF was reported to play an important role in visceral hypersensitivity in both patients with irritable bowel syndrome (IBS) and rodent model of IBS . NGF was also reported to be associated with gastric hypersensitivity in rats treated for colon inflammation .…”

Section: Introductionmentioning

confidence: 99%

Ameliorating effects of optimized gastric electrical stimulation and mechanisms involving nerve growth factor and opioids in a rodent model of gastric hypersensitivity

Yan

Yin

et al. 2019

Neurogastroenterology Motil

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Background Gastric electrical stimulation (GES) has been applied to treat gastric motility disorders for decades. This study was designed to investigate the effects and mechanisms of GES for visceral hypersensitivity in a rodent model of functional dyspepsia (FD). Methods Male Sprague‐Dawley rat pups at 10‐days old received 0.1% iodoacetamide (IA) daily for 6 days. The experiments were performed when the rats reached 8‐11 weeks of age, and visceral hypersensitivity was established. Then, GES parameters were optimized and the chronic effects of GES on gastric hypersensitivity were assessed by electromyogram (EMG). Naloxone (3 mg/kg), D‐Phe‐Cys‐Tyr‐D‐Trp‐Orn‐Thr‐Pen‐Thr‐NH2 (CTOP, 1 mg/kg), and anti‐NGF (16 μg/kg) were individually intraperitoneally injected to investigate opioid and nerve growth factor (NGF) mechanisms. Tissues were analyzed for NGF expression. Key Results In the IA‐treated rats, the visceromotor response to gastric distension was significantly increased, and both acute GES with optimized stimulation parameters (0.25 seconds on, 0.25 seconds off, 100 Hz, 0.25 ms, 6 mA) and chronic GES (7 days, 2 hours/day) normalized gastric hypersensitivity. The inhibitory effect of GES on gastric hypersensitivity was blocked by naloxone and CTOP. Anti‐NGF normalized EMG responses in IA‐treated rats. The expressions of NGF in the tissues of IA‐treated rats were dramatically increased, and these increases were suppressed with GES. Conclusions and Inferences GES with optimized parameters improves gastric hypersensitivity induced by neonatal treatment of IA mediated peripherally by suppressing NGF and via the opioid mechanism involving the µ receptor. GES as a potential therapy for treating visceral pain may be explored in clinical studies.

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Plasticity of dorsal root ganglion neurons in a rat model of post-infectious gut dysfunction: potential implication of nerve growth factor

Cited by 13 publications

References 32 publications

Antibiotic-induced dysbiosis alters host-bacterial interactions and leads to colonic sensory and motor changes in mice

Antibiotic-induced dysbiosis alters host-bacterial interactions and leads to colonic sensory and motor changes in mice

Persistent alterations in colonic afferent innervation in a rat model of postinfectious gut dysfunction: Role for changes in peripheral neurotrophic factors

Ameliorating effects of optimized gastric electrical stimulation and mechanisms involving nerve growth factor and opioids in a rodent model of gastric hypersensitivity

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