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Cross-Fostering Increases Th1/Th2 Expression in a Prenatal Dexamethasone Exposure Rat Model
Author(s) -
HoChang Kuo,
Mindy MingHuey Guo,
ShihFeng Liu,
ChihCheng Chen,
JiunnMing Sheen,
HongRen Yu,
MaoMeng Tiao,
YouLin Tain,
LiTung Huang
Publication year - 2014
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0115554
Subject(s) - dexamethasone , medicine , endocrinology , immune system , spleen , in utero , fetus , immunology , biology , pregnancy , genetics
Background Prenatal dexamethasone exposure has been reported to increase allergy potential in childhood possibly by interference with normal immunological development in utero . This study investigated the effects of prenatal dexamethasone on T helper cell immune responses in a rat model. Methods Pregnant rats received either dexamethasone 0.1 mg/kg/day or normal saline from gestational day 14–21. Off-springs were cared for by their biological mother, or cross-fostered by the opposing group. Spleen and blood samples were collected at post-natal day 7 and 120 and tested for mRNA expression and plasma cytokine levels of Th1/Th2/Th17 immune response. Results Both Th1 (T-bet) and Th2 (GATA-3) mRNA expression were shown to have a significant increase in the prenatal dexamethasone exposure group at day 120 (p<0.05). The plasma levels for Th1 (IFNγ and IL-2) and Th2 (IL-4, IL-5, IL-13) were found to have no significant differences between the two group (p>0.05). The mRNA expression of Th17 (RORγt) showed a significant decrease at post-natal day 120 as well as the plasma level of IL-17A at day 7 (11.21±1.67 vs. 6.23±1.06 pg/ml, p = 0.02). Cross-fostering by a dexamethasone exposed mother resulted in a significant increase in Th1/Th2 mRNA expression (p<0.05) and decrease of Th17. Conclusions Prenatal dexamethasone exposure increased Th1, Th2 and decreased Th17 expression. Cross-fostering by a dexamethasone exposed mother results in more prominent increase of Th1 and Th2 expression.

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