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Apoptosis of Intestinal Intraepithelial Lymphocytes Induced by Exogenous and Endogenous Glucocorticoids
Author(s) -
Murosaki Shinji,
InagakiOhara Kyoko,
Kusaka Hiroaki,
Ikeda Hitoshi,
Yoshikai Yasunobu
Publication year - 1997
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.1997.tb01179.x
Subject(s) - dexamethasone , intraepithelial lymphocyte , apoptosis , cd8 , biology , endocrinology , medicine , immunology , immune system , biochemistry
To investigate the effect of glucocorticoids on apoptosis in intestinal intraepithelial lymphocytes (i‐IEL), we examined the changes of i‐IEL followed by in vivo treatment with dexamethasone. The fragmented DNA of i‐IEL were significantly increased at 15 hr after dexamethasone treatment and, subsequently, the number of total i‐IEL were decreased by day 4 after treatment. Although all subsets of i‐IEL including CD8α/α + , CD8α/β + , CD4 + and CD4 + CD8 + i‐IEL were decreased after dexamethasone treatment, CD8α/α + i‐IEL appeared to be relatively resistant to dexamethasone‐induced apoptosis. Consistent with the in vivo findings, CD8α/α + i‐IEL exhibited less susceptibility to dexamethasone‐induced cell death in vitro than other subsets. To investigate whether this process occurs under physiological conditions, we examined the kinetics of i‐IEL after treatment with 15‐hr water immersion stress. In mice subjected to water immersion stress, plasma glucocorticoids were remarkably elevated soon after the 15‐hr stress. The increase in the fragmented DNA of i‐IEL and subsequent decrease in the number of i‐IEL were observed in the stressed mice in the same kinetics as seen in the dexamethasone‐treated mice. Similar to dexamethasone‐induced cell death, CD8α/α + i‐IEL appeared to be relatively resistant to stress‐induced apoptosis compared with other i‐IEL subsets. The expression level of Bcl‐2 was significantly higher in CD8α/α + i‐IEL than in CD8α/β + i‐IEL. Our results indicate that i‐IEL are subjected to cell death via apoptosis by exogenous and endogenous glucocorticoids and that different sensitivity to steroid‐induced apoptosis may exist among i‐IEL subsets in relation to their Bcl‐2 expression.