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Modulation of inflammatory and T hel...

Greeneltch, Kristy Markos.

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Modulation of inflammatory and T helper cell responses by opioids and IL-4: Direct effects on cytokine production, death effector expression, and activation-induced cell death.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Modulation of inflammatory and T helper cell responses by opioids and IL-4: Direct effects on cytokine production, death effector expression, and activation-induced cell death./
作者:	Greeneltch, Kristy Markos.
面頁冊數:	225 p.
附註:	Source: Dissertation Abstracts International, Volume: 65-09, Section: B, page: 4496.
Contained By:	Dissertation Abstracts International65-09B.
標題:	Health Sciences, Immunology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3147991
ISBN:	0496063510

Modulation of inflammatory and T helper cell responses by opioids and IL-4: Direct effects on cytokine production, death effector expression, and activation-induced cell death.
Greeneltch, Kristy Markos.

Modulation of inflammatory and T helper cell responses by opioids and IL-4: Direct effects on cytokine production, death effector expression, and activation-induced cell death. - 225 p.

Source: Dissertation Abstracts International, Volume: 65-09, Section: B, page: 4496.

Thesis (Ph.D.)--The George Washington University, 2004.

Chronic stress causes the release of opioids to promote an imbalance of cytokines and has been implicated in the onset of allergies, cancer and autoimmune diseases. The mechanisms by which opioids alter cytokine production to suppress the immune system are not clear. I found that administration of the opioid antagonist naltrexone inhibited lipopolysaccharide but not staphylococcal enterotoxin B or anti (alpha)-Fas antibody (Jo2)-mediated shock. Naltrexone significantly inhibited the production of TNF-alpha induced by LPS in vivo but did not have a direct effect on LPS-induced TNF-alpha production by macrophages in vitro nor on LPS-induced liver damage. These results suggest that naltrexone prevents LPS-induced mortality by indirect inhibition of TNF-alpha production in vivo.

ISBN: 0496063510Subjects--Topical Terms:

1017716
Health Sciences, Immunology.

Modulation of inflammatory and T helper cell responses by opioids and IL-4: Direct effects on cytokine production, death effector expression, and activation-induced cell death.
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245 1 0 $a Modulation of inflammatory and T helper cell responses by opioids and IL-4: Direct effects on cytokine production, death effector expression, and activation-induced cell death.
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500 $a Source: Dissertation Abstracts International, Volume: 65-09, Section: B, page: 4496.
500 $a Directors: Achsah D. Keegan; Yufang Shi.
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520 $a Chronic stress causes the release of opioids to promote an imbalance of cytokines and has been implicated in the onset of allergies, cancer and autoimmune diseases. The mechanisms by which opioids alter cytokine production to suppress the immune system are not clear. I found that administration of the opioid antagonist naltrexone inhibited lipopolysaccharide but not staphylococcal enterotoxin B or anti (alpha)-Fas antibody (Jo2)-mediated shock. Naltrexone significantly inhibited the production of TNF-alpha induced by LPS in vivo but did not have a direct effect on LPS-induced TNF-alpha production by macrophages in vitro nor on LPS-induced liver damage. These results suggest that naltrexone prevents LPS-induced mortality by indirect inhibition of TNF-alpha production in vivo.
520 $a In in vitro models, chronic morphine administration alters cytokine production by T cells and also enhances Fas expression. In this study, I analyzed the role of morphine in promoting Th2 differentiation via enhancement of Fas, FasL or TRAIL, to promote killing of Th1 cells. I found that morphine promoted Th2 development as evidenced by increased IL-4 and IL-13 production, and also enhanced death effector expression in CD4+ T cells. Naltrexone inhibited morphine-induced gene expression and cytokine production indicating that morphine causes its effects by binding to a classical opioid receptor. Blockade of Fas/FasL interaction using anti-FasL inhibited morphine-promoted IL-4, IL-13 and AICD. These results suggest that morphine enhances Th2 differentiation via killing of Th1 cells in a FasL-dependent manner.
520 $a To further investigate molecular factors involved in Th2 skewing, the ability of IRS-2 to enhance AICD of Th1 cells was examined. CD4+ T cells from IRS-2 transgenic mice were cultured under neutral, Th1 and Th2 conditions. Overexpression of IRS-2 promoted IL-5 and IL-13 production however IRS-2 did not enhance Th2 development per se as it did not enhance IL-4 production. The mRNA expression of GATA-3 under the three conditions did not directly correlate with observed changes in cytokine production. The IRS-2 transgene was also found to enhance Fas, FasL and TRAIL expression in Th1 cells. IRS-2 promoted AICD of T cells under neutral conditions and this effect was FasL-dependent, indicating that the majority of apoptotic cells were likely Th1.
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