Effect of cholecystokinin receptor blockade on human lymphocyte proliferation

J Surg Res. 1990 Apr;48(4):354-7. doi: 10.1016/0022-4804(90)90074-c.

Abstract

Cholecystokinin is a peptide produced by neuroendocrine cells in gut and neurons in brain and gut. Proliferating human peripheral blood mononuclear cells (H-PBMC) also make small amounts of cholecystokinin. Cholecystokinin increases intracellular calcium (Ca2+) in H-PBMC. This can be blocked with L 364, 718, a non-toxic specific cholecystokinin antagonist. Cholecystokinin is a comitogen for H-PBMC and activates H-PBMC in a cyclosporine-resistant fashion. If cholecystokinin is a critical lymphokine, then L 364, 718 should block H-PBMC mitogenesis. H-PBMC from healthy donors were stimulated in vitro with either phytohemagglutinin or anti-CD3 monoclonal antibody. L 364, 718 was not toxic for H-PBMC, yet inhibited mitogenesis at 10(-7), 10(-6), and 10(-5) M. The small amount of cholecystokinin made by H-PBMC may play a critical role in H-PBMC mitogenesis.

MeSH terms

  • Antibodies, Monoclonal
  • Antigens, CD / immunology
  • Benzodiazepinones / pharmacology
  • Cell Division
  • Cholecystokinin / antagonists & inhibitors
  • Devazepide
  • Humans
  • Lymphocytes / cytology*
  • Lymphocytes / metabolism
  • Phytohemagglutinins
  • Receptors, Cholecystokinin / physiology*
  • Thymidine / metabolism

Substances

  • Antibodies, Monoclonal
  • Antigens, CD
  • Benzodiazepinones
  • Phytohemagglutinins
  • Receptors, Cholecystokinin
  • Cholecystokinin
  • Devazepide
  • Thymidine