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Expression of aryl hydrocarbon receptor and ATG16L1 protein in experimental oxazolone-induced colitis in rats
Abstract:
We studied the expression of AhR and ATG16L1 protein in experimental oxazolone-induced colitis in rats and anti-inflammatory action of recombinant antagonist of IL-1 receptors (ARIL-1) and simvastatin. The immunopositive cells were determined using an indirect immunofluorescence technique with using a monoclonal rat antibody. It has been established that development of colitis was accompanied by an increase of total number of ATG16L1-lymphocytes (by 30%, P < 0.05) in lymphoid structures of the colon. However the amount of AhR(+)-lymphocytes has not changed. At the same time has increased the concentration of ATG16L1 protein (by 4-11%, P < 0.05) in immunopositive cells. Administration of simvastatin and ARIL-1 during the development of experimental pathology was accompanied by decrease of total number of AhR(+) (by 24-38%, P < 0.05) and ATG16L1(+)-lymphocytes (by 43% - 2 fold, P < 0.05) in the colon.
Insights
Experimental colitis in rats showed increased ATG16L1-lymphocytes and protein levels. Treatments with ARIL-1 and simvastatin reduced both AhR(+) and ATG16L1(+) lymphocytes, indicating anti-inflammatory effects.
Area of Science:
- Immunology
- Gastroenterology
- Pharmacology
Background:
- Oxazolone-induced colitis is a model for inflammatory bowel disease.
- The role of Aryl hydrocarbon receptor (AhR) and ATG16L1 in colitis pathogenesis requires further elucidation.
Purpose of the Study:
- To investigate the expression of AhR and ATG16L1 in experimental colitis.
- To evaluate the anti-inflammatory effects of recombinant antagonist of IL-1 receptors (ARIL-1) and simvastatin on these markers.
Main Methods:
- Experimental colitis was induced using oxazolone in rats.
- Immunofluorescence technique with monoclonal antibodies was used to quantify AhR and ATG16L1 positive cells.
- ARIL-1 and simvastatin were administered during colitis development.
Main Results:
- Colitis development led to a significant increase in ATG16L1-lymphocytes (30%) and ATG16L1 protein concentration (4-11%).
- AhR(+) lymphocyte counts remained unchanged during colitis.
- Treatment with ARIL-1 and simvastatin significantly decreased both AhR(+) (24-38%) and ATG16L1(+) lymphocytes (43%-2 fold).
Conclusions:
- ATG16L1 expression is upregulated in experimental colitis.
- ARIL-1 and simvastatin exhibit anti-inflammatory properties by reducing AhR and ATG16L1 positive lymphocytes in the colon.
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