Cross-fostering increases Th1/Th2 expression in a prenatal dexamethasone exposure rat model

Ho Chang Kuo*, Mindy Ming Huey Guo, Shih Feng Liu, Chih Cheng Chen, Jiunn Ming Sheen, Hong Ren Yu, Mao Meng Tiao, You Lin Tain, Li Tung Huang

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

3 Scopus citations

Abstract

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, p50.02). 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.

Original languageEnglish
Article numbere115554
JournalPLoS ONE
Volume9
Issue number12
DOIs
StatePublished - 19 12 2014

Bibliographical note

Publisher Copyright:
© 2014 Kuo et al.

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