VITAMIN-A AND RETINOIC ACIDS IMMUNOMODULATION ON HUMAN GUT LYMPHOCYTES

Citation
Y. Elitsur et al., VITAMIN-A AND RETINOIC ACIDS IMMUNOMODULATION ON HUMAN GUT LYMPHOCYTES, Immunopharmacology, 35(3), 1997, pp. 247-253
Citations number
35
Categorie Soggetti
Pharmacology & Pharmacy",Immunology
Journal title
ISSN journal
01623109
Volume
35
Issue
3
Year of publication
1997
Pages
247 - 253
Database
ISI
SICI code
0162-3109(1997)35:3<247:VARAIO>2.0.ZU;2-N
Abstract
Epidemiological studies have suggested an important immunomodulatory r ole for vitamin A and other related vitamin A compounds in adults and children. Although vitamin A is absorbed via the gastrointestinal trac t, its affect on the gut mucosal immune cells has not been adequately investigated. We investigated the in-vitro effect of vitamin A (retino l) and its retinoid acid (RA) compounds (13-cis- and all tuans-retinoi c acids) on the human gut mucosal immune system as represented by colo nic lamina propria lymphocyte (LPL) proliferation, and ornithine decar boxylase (ODC) activity. Results showed that retinol suppressed and tr ans-retinoic acid enhanced thymidine incorporation into LPL. 13-cis re tinoic acid did not significantly affect LPL DNA synthesis. Similarly, retinol (0.025 mu g/ml and 10 mu g/ml) and 13-cis retinoic acid(conc. 10 mu g/ml) suppressed, while all trans-retinoic acid (cone. 10 mu g/ ml) enhanced ODC activity in PHA-stimulated LPL. Interestingly, the ef fects of retinol and all trans-RA were abolished when LPL were previou sly depleted of macrophages. Addition of monocyte-associated lymphokin es, IL-1 and 1L-6, showed that IL-1 partially replaced the enhancing e ffect of all trans-RA previously observed on LPL thymidine incorporati on. IL-6 did not affect LPL DNA synthesis irrespective of the vitamin A compound used. We conclude that retinol and retinoid acids (13-cis, all trans-) may alter the human colonic immune system possibly via IL1 cytokine, but not via IL-6, The data suggest that vitamin A and its r etinoid compounds may participate in the modulation of the gut immune system.