Plasticity of dorsal root ganglion neurons in a rat model of post-infectious gut dysfunction: potential implication of nerve growth factor
Abstract
OBJECTIVE: Intestinal infections are suggested as a risk factor for the development of irritable bowel syndrome (IBS)-like visceral hypersensitivity. The mechanisms implicated might involve long-term changes in visceral afferents, with implication of nerve growth factor (NGF). We explored plastic changes in dorsal root ganglia (DRGs) receiving innervation from the gut and the potential implication of NGF in a rat model of IBS-like post-infectious gut dysfunction. MATERIALS AND METHODS: Rats were infected with Trichinella spiralis larvae. Thirty days post-infection, inflammatory markers, including interleukins (ILs) and mucosal mast cell infiltration (rat mast cell protease II [RMCPII]), and NGF and TrkA expression was determined in the jejunum and colon (RT-qPCR). In the same animals, morphometry (neuronal body size) and NGF content (immunofluorescence) were assessed in thoracolumbar DRG neurons. RESULTS: In infected animals, a low-grade inflammatory-like response, characterized by up-regulated levels of RMCPII and IL-6, was observed in the jejunum and colon. TrkA expression was increased in the jejunum, whereas the colon showed a slight reduction. NGF levels remained unaltered regardless the gut region. Overall, the mean cross-sectional area of DRG neurons was increased in T. spiralis-infected animals, with a reduction in both TrkA and NGF staining. CONCLUSIONS: Results suggest that during T. spiralis infection in rats, there is a remodeling of sensory afferents that might imply a NGF-mediated mechanism. Plastic changes in sensory afferents might mediate the long-lasting functional alterations that characterize this model of IBS. Similar mechanisms might be operating in patients with post-infectious-IBS.
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NGF has been implicated in the sensitization of visceral afferents, leading to the development of hypersensitivity.
“Additionally, NGF has been implicated in the sensitization of visceral afferents, leading to the development of hypersensitivity.46”
From Antibiotic-induced dysbiosis alters host-bacterial interactions and leads to colonic sensory and motor changes in mice (2015) · cites this paper as [46]
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- Authors
- Jardí, F., Fernández-Blanco, J. A., Martínez, V., & Vergara, P.
- Affiliations
- Universitat Autònoma de Barcelona (ES)
- Department of Cell Biology, Physiology and Immunology, Universitat Autònoma de Barcelona, Barcelona, Spain
- Venue
- Scandinavian Journal of Gastroenterology
- Publisher
- Informa UK Limited
- Published
- 2014-09-26
- Volume
- 49
- Issue
- 11
- Pages
- 1296-1303
- ISSN
- 0036-5521 (ISSN-L)
- 1502-7708
- OpenAlex
- W2082586056
- Cited by
- 15
- References
- 32
- Citations by year
- 2026: 1 · 2025: 1 · 2022: 1 · 2019: 2 · 2018: 2 · 2016: 4 · 2015: 3 · 2014: 1
- FWCI
- 2.67
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Scandinavian Journal of Gastroenterology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Generalitat de Catalunya
- Topics
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Vagus Nerve Stimulation Research
- Keywords
- dorsal root ganglion neurons, nerve growth factor, TrkA, Trichinella spiralis infection, post-infectious irritable bowel syndrome, visceral hypersensitivity, intestinal inflammation, mast cells, interleukin-6, intestinal infection
- MeSH terms
- Animals, Colitis, Disease Models, Animal, Ganglia, Spinal, Male, Neuronal Plasticity, Rats, Sprague-Dawley, Nerve Growth Factor, Irritable Bowel Syndrome, Rats
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