Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 139-148 |
| Number of pages | 10 |
| Journal | MICROBIOLOGY and IMMUNOLOGY |
| Volume | 41 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - Jan 1 1997 |
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All Science Journal Classification (ASJC) codes
- Microbiology
- Immunology
- Virology
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Apoptosis of intestinal intraepithelial lymphocytes induced by exogenous and endogenous glucocorticoids. / Murosaki, Shinji; Inagaki-Ohara, Kyoko; Kusaka, Hiroaki; Ikeda, Hitoshi; Yoshikai, Yasunobu.
In: MICROBIOLOGY and IMMUNOLOGY, Vol. 41, No. 2, 01.01.1997, p. 139-148.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Apoptosis of intestinal intraepithelial lymphocytes induced by exogenous and endogenous glucocorticoids
AU - Murosaki, Shinji
AU - Inagaki-Ohara, Kyoko
AU - Kusaka, Hiroaki
AU - Ikeda, Hitoshi
AU - Yoshikai, Yasunobu
PY - 1997/1/1
Y1 - 1997/1/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0031049735&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0031049735&partnerID=8YFLogxK
U2 - 10.1111/j.1348-0421.1997.tb01179.x
DO - 10.1111/j.1348-0421.1997.tb01179.x
M3 - Article
C2 - 9087956
AN - SCOPUS:0031049735
VL - 41
SP - 139
EP - 148
JO - Microbiology and Immunology
JF - Microbiology and Immunology
SN - 0385-5600
IS - 2
ER -