Fetal alcohol exposure attenuates interleukin-1β-induced fever: Neuroimmune mechanisms

Anna N. Taylor; Delia L. Tio; Raz Yirmiya

doi:10.1016/S0165-5728(99)00102-2

Fetal alcohol exposure attenuates interleukin-1β-induced fever: Neuroimmune mechanisms

Anna N. Taylor^*, Delia L. Tio, Raz Yirmiya

^*Corresponding author for this work

Department of Psychology

Research output: Contribution to journal › Article › peer-review

20 Scopus citations

Abstract

Central mechanisms for the attenuating effects of fetal alcohol exposure (FAE) on interleukin-1β (IL-1)-induced fever were studied in adult male offspring of dams fed a liquid diet supplemented with ethanol (E), in pair- fed (P) control and in normal (N) offspring. Hypothalamic levels of IL-1 were significantly lower in E than in N rats at 2 h, but not at 4 and 6 h, after intraperitoneal administration of lipopolysaccharide. Fever induced by intracerebroventricular (icv) IL-1 was significantly lower in E than in N and P rats. In contrast, E rats showed a normal febrile response to icv prostaglandin-E₂. Thus, whereas FAE does not affect central thermoregulatory mechanisms, per se, FAE alters the kinetics of hypothalamic IL-1 production/appearance and decreases the responsiveness of central mechanisms which mediate the febrile response to IL-1.

Original language	English
Pages (from-to)	44-52
Number of pages	9
Journal	Journal of Neuroimmunology
Volume	99
Issue number	1
DOIs	https://doi.org/10.1016/S0165-5728(99)00102-2
State	Published - 1 Sep 1999

Bibliographical note

Funding Information:
We thank Dr. Deborah M. Hodgson, Mr. Ngy Heng and Ms. Patricia P.Y. Lee for their contributions to this study. Supported by grants from the NIH/NIAAA (AA09850) and the Department of Veterans Affairs Medical Research Service (A.N.T.) and by the United States–Israel Binational Science Foundation 94-62 (R.Y. and A.N.T.).

Keywords

Brain
Fetal alcohol exposure
Fever
Interleukin-1β
Prostaglandin-E
Rat
Sickness behavior

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10.1016/S0165-5728(99)00102-2

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title = "Fetal alcohol exposure attenuates interleukin-1β-induced fever: Neuroimmune mechanisms",

abstract = "Central mechanisms for the attenuating effects of fetal alcohol exposure (FAE) on interleukin-1β (IL-1)-induced fever were studied in adult male offspring of dams fed a liquid diet supplemented with ethanol (E), in pair- fed (P) control and in normal (N) offspring. Hypothalamic levels of IL-1 were significantly lower in E than in N rats at 2 h, but not at 4 and 6 h, after intraperitoneal administration of lipopolysaccharide. Fever induced by intracerebroventricular (icv) IL-1 was significantly lower in E than in N and P rats. In contrast, E rats showed a normal febrile response to icv prostaglandin-E2. Thus, whereas FAE does not affect central thermoregulatory mechanisms, per se, FAE alters the kinetics of hypothalamic IL-1 production/appearance and decreases the responsiveness of central mechanisms which mediate the febrile response to IL-1.",

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note = "Funding Information: We thank Dr. Deborah M. Hodgson, Mr. Ngy Heng and Ms. Patricia P.Y. Lee for their contributions to this study. Supported by grants from the NIH/NIAAA (AA09850) and the Department of Veterans Affairs Medical Research Service (A.N.T.) and by the United States–Israel Binational Science Foundation 94-62 (R.Y. and A.N.T.).",

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AB - Central mechanisms for the attenuating effects of fetal alcohol exposure (FAE) on interleukin-1β (IL-1)-induced fever were studied in adult male offspring of dams fed a liquid diet supplemented with ethanol (E), in pair- fed (P) control and in normal (N) offspring. Hypothalamic levels of IL-1 were significantly lower in E than in N rats at 2 h, but not at 4 and 6 h, after intraperitoneal administration of lipopolysaccharide. Fever induced by intracerebroventricular (icv) IL-1 was significantly lower in E than in N and P rats. In contrast, E rats showed a normal febrile response to icv prostaglandin-E2. Thus, whereas FAE does not affect central thermoregulatory mechanisms, per se, FAE alters the kinetics of hypothalamic IL-1 production/appearance and decreases the responsiveness of central mechanisms which mediate the febrile response to IL-1.

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Fetal alcohol exposure attenuates interleukin-1β-induced fever: Neuroimmune mechanisms

Abstract

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Keywords

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