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Intestinal neuro-epithelial interactions modulate neuronal chemokines production
Emmanuelle Tixier1, Jean-Paul Galmiche, Michel Neunlist
1Institut National de la Santé et de la Recherche Médicale U539, Hôpital Hôtel-Dieu, 44093 Nantes, France.
Biochemical and Biophysical Research Communications
|April 20, 2006
Summary
Human enteric neurons produce chemokines during gut inflammation, influenced by neuro-epithelial interactions. Neurons can attract immune cells, potentially driving inflammation in the enteric nervous system.
Area of Science:
- Neuroscience
- Immunology
- Gastroenterology
Background:
- Human enteric neurons can produce chemokines during intestinal inflammation.
- The role of neuro-epithelial interactions in modulating neuronal chemokine production is unclear.
- The capacity of enteric neurons to induce immune cell chemotaxis is unknown.
Purpose of the Study:
- To investigate if neuro-epithelial interactions modulate neuronal chemokine production.
- To determine if enteric neurons can induce immune cell chemotaxis.
- To elucidate the mechanisms underlying these interactions in intestinal inflammation.
Main Methods:
- Utilized a coculture model of human neurons (NT2-N) and intestinal epithelial cells (Caco-2).
- Analyzed chemokine (IL-8, MIP-1beta) expression via quantitative-PCR, ELISA, and immunohistochemistry.
- Assessed neuronally induced chemotaxis using cocultures of NT2-N and human peripheral blood mononuclear cells (PBMC).
Main Results:
- Caco-2 inflammation significantly increased neuronal IL-8 and MIP-1beta mRNA expression.
- This increase was attenuated by IL-1 receptor antagonist, indicating IL-1beta involvement.
- IL-1beta-primed neurons induced PBMC chemotaxis, partially mediated by IL-8.
Conclusions:
- Neuro-epithelial interactions modulate neuronal chemokine production via IL-1beta-dependent pathways during inflammation.
- Neuronal IL-1beta can induce immune cell chemotaxis, potentially contributing to immune infiltrates in the enteric nervous system.
- Findings suggest a role for enteric neurons in immune cell recruitment during intestinal inflammation.
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