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Growth hormone and IBD: Reduction of intestinal inflammation, promotion of growth

intestine, as well as promoting growth.

In the long run, "this may lead to new therapeutic approaches which will take advantage of these properties in both improving growth and intestinal healing in IBD," Dr. Denson noted.

Background and results

STAT3 (signal transducer and activator of transcription-3) regulates disease activity in experimental colitis and human IBD. Suppressor of cytokine signaling 3 (SOCS-3) and Src-homology tyrosine phosphatase 2 (SHP2) are negative regulators of Il-6 dependent STAT3 activation via the gp130 receptor. Growth hormone (GH) reduces disease activity in experimental colitis, however, the molecular mechanism was not known.

The researchers hypothesized that "GH would ameliorate colitis by upregulating SOCS-3 or SHP2 and reducing STAT3 activation." Their experiment showed that GH administration indeed did improve weight gain and colon histopathology in IL-10 null mice with colitis. This wasn't associated with increases in either serum or colon IGF-1.

GH increased apoptosis of lamina propria mononuclear cells (LPMC), while reducing apoptosis and increasing proliferation of crypt epithelial cells (CEC). GH reduced STAT3 activation in both CEC and LPMC; the improvement in histopathology was associated with reduced STAT3 activation. Growth hormone also enhanced SHP2:gp130 binding under these conditions, while SOCS-3 abundance was reduced.

Direct effects of GH were investigated in tissue culture. Growth hormone treatment decreased constituitive STAT3 activation in IL-10 null mouse colon organ culture. As was observed in vivo, GH increased SHP2:gp130 association and reduced IL-6 dependent STAT3 activation in T84 human colon carcinoma cells.

Conclusion

The Cincinnati investigators found that growth hormone administration improved weight gain and reduced disease activity in IL-10 null mice with colitis. This was related to a reduction in STAT3 activation associa
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10-Sep-2004


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