Apoptosis of intestinal intraepithelial lymphocytes induced by exogenous and endogenous glucocorticoids

Shinji Murosaki, Kyoko Inagaki-Ohara, Hiroaki Kusaka, Hitoshi Ikeda, Yasunobu Yoshikai

    Research output: Contribution to journalArticle

    28 Citations (Scopus)

    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 languageEnglish
    Pages (from-to)139-148
    Number of pages10
    JournalMICROBIOLOGY and IMMUNOLOGY
    Volume41
    Issue number2
    DOIs
    Publication statusPublished - Jan 1 1997

    Fingerprint

    Glucocorticoids
    Lymphocytes
    Apoptosis
    Dexamethasone
    Cell Death
    Lymphocyte Subsets
    Immersion
    Dehydration
    DNA
    Steroids

    All Science Journal Classification (ASJC) codes

    • Microbiology
    • Immunology
    • Virology

    Cite this

    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 journalArticle

    Murosaki, Shinji ; Inagaki-Ohara, Kyoko ; Kusaka, Hiroaki ; Ikeda, Hitoshi ; Yoshikai, Yasunobu. / Apoptosis of intestinal intraepithelial lymphocytes induced by exogenous and endogenous glucocorticoids. In: MICROBIOLOGY and IMMUNOLOGY. 1997 ; Vol. 41, No. 2. pp. 139-148.
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    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.",
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