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Intestinal intraepithelial lymphocytes influence the production of somatostatin
D H Teitelbaum1, J Del Valle, B Reyas
1Department of Surgery, University of Michigan Medical Center, Ann Arbor, USA.
Background:
We have previously demonstrated that intestinal intraepithelial lymphocytes (iIELs) inhibit lymphocyte proliferation. Because somatostatin also prevents lymphocyte proliferation, we hypothesized that iIELs may influence production of somatostatin.
Methods:
Isolates of intestinal epithelium that were obtained from Brown Norway (BN) rats and contained an iIEL-enriched population (defined as CD45+) were incubated with irradiated Lewis splenocytes for allogeneic stimulation. BN rat splenocytes incubated with irradiated Lewis splenocytes served as a control. Supernatants were harvested after 4 days and assayed for somatostatin by using a radioimmunoassay.
Results:
The somatostatin level in the intestinal epithelium-conditioned supernatant was significantly higher than that of the control group (176 +/- 60 versus 10 +/- 2 fmol/ml; p < 0.05). Removal of the CD45+ cell subset resulted in a fifteenfold reduction in somatostatin levels. The CD45+ cell lysates had significantly higher levels of somatostatin than did CD45+ depleted cells (1304 +/- 531 versus 128 +/- 41 fmol/ml; p < 0.05).
Conclusions:
The isolates of intestinal epithelium produced significant amounts of somatostatin. Removal of the CD45+ cells caused a significant loss of somatostatin production. Intracellular levels of somatostatin appeared to be highest in the CD45+ subpopulation. These data suggest that iIELs (that is, CD45+ cells) may have a significant influence on the production of somatostatin and may be a source of somatostatin production. Production of somatostatin by iIELs may help modulate immune responses in gut-associated lymphoid tissue.