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Adrenal cortical activation in murine colitis.
D Franchimont1, G Bouma, J Galon
1Pediatric and Reproductive Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892, USA.
Gastroenterology
|December 13, 2000
Summary
Inflammatory bowel disease, specifically colitis, causes significant adrenal gland enlargement and increased corticosterone. Direct immune cell interactions with adrenal cells, particularly involving interleukin-6, drive this response.
Area of Science:
- Endocrinology
- Immunology
- Gastroenterology
Background:
- Adrenal glucocorticoid secretion is vital for managing inflammatory diseases.
- The adrenal gland's role in inflammatory bowel diseases (IBD) remains under-investigated.
Purpose of the Study:
- To investigate adrenal gland function and structure in a mouse model of colitis.
- To explore the mechanisms underlying adrenal activation during inflammatory bowel disease.
Main Methods:
- Induced trinitrobenzene sulfonic acid (TNBS) colitis in SJL/J mice.
- Analyzed plasma hormone and cytokine levels, adrenal structure (immunohistochemistry, electron microscopy), and gene expression (RNase protection).
Main Results:
- Colitic mice exhibited enlarged, hypervascularized adrenal glands with stimulated adrenocortical cells.
- Plasma corticosterone levels significantly increased, correlating with elevated interleukin-6 (IL-6) and intra-adrenal IL-6 expression.
- Direct contact between intra-adrenal lymphocytes and adrenocortical cells was observed; anti-IL-6 antibody treatment mitigated adrenal activation.
Conclusions:
- Colitis profoundly stimulates adrenocortical cell function and glucocorticoid release.
- Direct immune-adrenal interactions, mediated by IL-6, play a key role in adrenal gland activation during colitis.
