Intestinal intraepithelial lymphocytes influence the production of somatostatin.

Abstract

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. 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. 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). 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.