Abstract
To clarify whether corticotropin releasing hormone (CRH) and β-endorphin (βEP) system mediate maternal immunosuppression in pregnant rats exposed to heat through central or placental pathway, we examined the effects of intravenous (iv) (100 or 500 μg) or intracerebroventricular (icv) (5μg) administration of CRH receptor antagonist α-helical CRH (9-41) on splenic natural killer cell activity (NKCA) as well as βEP in blood, pituitary lobes, and placenta in pregnant rats at 15 to 16 days gestation. Two-way ANOVA revealed that heat reduced NKCA and elevated blood and pituitary βEP but did not change placental βEP. Iv administered 500 μg and icv administered α-helical CRH reversed the reduced NKCA and the elevated pituitary βEP, while iv administration of 100 μg α-helical CRH did not. The increased blood βEP was reversed by iv 100 and 500 μg α-helical CRH and icv administration. Both iv and icv administrations reduced placental βEP independent of heat exposure. Thus, the response of placental βEP to iv administration of α-helical CRH seemed to be stronger than that of pituitary βEP. These results indicate that α-helical CRH which acts on pituitary βEP antagonizes heat-induced immunosuppression during pregnancy, suggesting that immunosuppression produced by heat stress during pregnancy is mediated by the central CRH system. The placental CRH-βEP system seems unlikely to be involved in the immunosuppression. Physiologic roles of placental CRH and opioid system should be clarified by future in vitro experiments using placenta specimen including placental immunocyte.
| Original language | English |
|---|---|
| Pages (from-to) | 43-53 |
| Number of pages | 11 |
| Journal | Brain, Behavior, and Immunity |
| Volume | 15 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 2001 |
| Externally published | Yes |
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Keywords
- β-endorphin
- CRH
- Natural killer cell activity
- Pituitary
- Placenta
ASJC Scopus subject areas
- Immunology
- Behavioral Neuroscience
- Endocrine and Autonomic Systems
Cite this
Involvement of central, but not placental corticotropin releasing hormone (CRH) in heat stress induced immunosuppression during pregnancy. / Nakamura, Hiroyuki; Nagase, Hirofumi; Ogino, Keiki; Hatta, Kotaro; Matsuzaki, Ichiyo.
In: Brain, Behavior, and Immunity, Vol. 15, No. 1, 2001, p. 43-53.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Involvement of central, but not placental corticotropin releasing hormone (CRH) in heat stress induced immunosuppression during pregnancy
AU - Nakamura, Hiroyuki
AU - Nagase, Hirofumi
AU - Ogino, Keiki
AU - Hatta, Kotaro
AU - Matsuzaki, Ichiyo
PY - 2001
Y1 - 2001
N2 - To clarify whether corticotropin releasing hormone (CRH) and β-endorphin (βEP) system mediate maternal immunosuppression in pregnant rats exposed to heat through central or placental pathway, we examined the effects of intravenous (iv) (100 or 500 μg) or intracerebroventricular (icv) (5μg) administration of CRH receptor antagonist α-helical CRH (9-41) on splenic natural killer cell activity (NKCA) as well as βEP in blood, pituitary lobes, and placenta in pregnant rats at 15 to 16 days gestation. Two-way ANOVA revealed that heat reduced NKCA and elevated blood and pituitary βEP but did not change placental βEP. Iv administered 500 μg and icv administered α-helical CRH reversed the reduced NKCA and the elevated pituitary βEP, while iv administration of 100 μg α-helical CRH did not. The increased blood βEP was reversed by iv 100 and 500 μg α-helical CRH and icv administration. Both iv and icv administrations reduced placental βEP independent of heat exposure. Thus, the response of placental βEP to iv administration of α-helical CRH seemed to be stronger than that of pituitary βEP. These results indicate that α-helical CRH which acts on pituitary βEP antagonizes heat-induced immunosuppression during pregnancy, suggesting that immunosuppression produced by heat stress during pregnancy is mediated by the central CRH system. The placental CRH-βEP system seems unlikely to be involved in the immunosuppression. Physiologic roles of placental CRH and opioid system should be clarified by future in vitro experiments using placenta specimen including placental immunocyte.
AB - To clarify whether corticotropin releasing hormone (CRH) and β-endorphin (βEP) system mediate maternal immunosuppression in pregnant rats exposed to heat through central or placental pathway, we examined the effects of intravenous (iv) (100 or 500 μg) or intracerebroventricular (icv) (5μg) administration of CRH receptor antagonist α-helical CRH (9-41) on splenic natural killer cell activity (NKCA) as well as βEP in blood, pituitary lobes, and placenta in pregnant rats at 15 to 16 days gestation. Two-way ANOVA revealed that heat reduced NKCA and elevated blood and pituitary βEP but did not change placental βEP. Iv administered 500 μg and icv administered α-helical CRH reversed the reduced NKCA and the elevated pituitary βEP, while iv administration of 100 μg α-helical CRH did not. The increased blood βEP was reversed by iv 100 and 500 μg α-helical CRH and icv administration. Both iv and icv administrations reduced placental βEP independent of heat exposure. Thus, the response of placental βEP to iv administration of α-helical CRH seemed to be stronger than that of pituitary βEP. These results indicate that α-helical CRH which acts on pituitary βEP antagonizes heat-induced immunosuppression during pregnancy, suggesting that immunosuppression produced by heat stress during pregnancy is mediated by the central CRH system. The placental CRH-βEP system seems unlikely to be involved in the immunosuppression. Physiologic roles of placental CRH and opioid system should be clarified by future in vitro experiments using placenta specimen including placental immunocyte.
KW - β-endorphin
KW - CRH
KW - Natural killer cell activity
KW - Pituitary
KW - Placenta
UR - http://www.scopus.com/inward/record.url?scp=0035174273&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0035174273&partnerID=8YFLogxK
U2 - 10.1006/brbi.2000.0591
DO - 10.1006/brbi.2000.0591
M3 - Article
C2 - 11259079
AN - SCOPUS:0035174273
VL - 15
SP - 43
EP - 53
JO - Brain, Behavior, and Immunity
JF - Brain, Behavior, and Immunity
SN - 0889-1591
IS - 1
ER -