Peer-reviewed veterinary case report
The influence of experimental ileitis on the neuropeptide coding of enteric neurons in the pig.
- Journal:
- Polish journal of veterinary sciences
- Year:
- 2005
- Authors:
- Czaja, K et al.
- Affiliation:
- Department of Animal Anatomy
Abstract
In the present study, both the ELISA test and immunohistochemical staining were used to investigate the influence of artificially induced ileitis on the chemical coding of enteric neurons in the pig. The ileum wall in experimental (E) pigs was injected in multiple sites with 4% paraformaldehyde to induce inflammation, while in the control (C) animals, the organ was injected with 0.1M phosphate buffer (pH 7.4). Three days after ileitis induction, samples of ileum wall from all the animals were evaluated for VIP, SP, CGRP, NPY, GAL and SOM concentration (ELISA test) and the expression of these biologically active substances by the enteric neurons (immunohistochemical staining). Quantitative results showed that ileitis decreased tissue concentration of VIP, CGRP and SOM but increased tissue concentration of SP, NPY and GAL. Immunochemistry revealed that in both the experimental and control pigs, VIP-positive (VIP+) nerve fibers supplied mainly ileal blood vessels, and the labeled pericarya were located in the inner (ISP) and outer submucous plexus (OSP). SP+ and CGRP+ nerve terminals were found in both the mucous and muscular membrane, while the labeled pericarya were found in ISP, OSP and myenteric plexus (MP). In both C and E pigs, the very few nerve terminals containing NPY and SOM were located mainly in the mucous membrane. NPY- or/and SOM-immunopositive nerve cell bodies were found in ISP, OSP and MP. GAL+ nerve fibers supplied all layers of the ileum and were most numerous in the muscular membrane, while the labeled pericarya were present in all the enteric plexuses. The present results suggest that enteric neurons are highly plastic in their response to inflammation.
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Search related cases →Original publication: https://pubmed.ncbi.nlm.nih.gov/15989136/