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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Prenatal manipulations reduce the proinflammatory response to a cytokine challenge in juvenile monkeys.

Two studies were conducted to assess the potential long-term effects of prenatal stress on the cytokine-related inflammatory response in juvenile rhesus monkeys. Subjects were derived from two different pregnancy conditions. Study 1 involved endocrine activation of the pregnant female by daily adrenocorticotropic hormone (ACTH) injection across a 2-week period (days 120-133 post-conception). Pregnant females in Study 2 experienced a psychological stressor, 10 minutes per day, for a 6-week period (days 106-147 post-conception). When the offspring from these pregnancies were 1.5-2 years of age, they were administered recombinant human interleukin-1beta (rhIL-1beta) to stimulate the release of endogenous cytokines, elicit fever, and activate the hypothalamic-pituitary-adrenal (HPA) axis. Cerebrospinal fluid (CSF) and blood levels of interleukin-6 (IL-6) were measured, as well as cortisol levels and body temperature. The prenatal ACTH treatment altered the postnatal response to IL-1beta in juvenile offspring. These monkeys showed a significantly blunted response to the IL-1beta, with smaller increments in blood and CSF levels of IL-6 and diminished temperature responses to the IL-1beta. In contrast, the prenatal psychological stressor was not as potent and did not have lasting effects on this physiological response in juvenile monkeys. IL-1beta also induced significant increases in cortisol secretion, but this adrenal response was comparable in all monkeys. These data suggest that differences in the prenatal environment could have a selective effect on cytokine physiology accounting for individual differences in the inflammatory response.[1]


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