title: Effects of lipopolysaccharide exposure at different postnatal time points on the response of LH to homotypic stress in adulthood.
abstract: Early-life immune stress may have long-lasting effects, known as programming effects, on the physiological response to stress in adulthood. There may be a critical window after birth during which such a challenge can induce long-lasting alterations. However, there are few reports regarding the consequences of this phenomenon for later reproductive function. Here we report on induction by early-life LPS injection of long-lasting alterations in the adult LH response to homotypic immune stress in male rats. First, we investigated developmental changes in the LH response to LPS, since immune challenge during the stress hyporesponsive period can induce long-lasting effects on physiological functions. Rat serum LH concentrations were decreased by LPS (100 μg/kg) injection on postnatal day 15 or 25, but not day 10, suggesting that the period prior to postnatal day 10 is the stress hyporesponsive period for LH. Serum LH concentrations and body weight were decreased by adult LPS (400 μg/kg) injection in rats given saline or LPS (100 μg/kg) on postnatal day 25, but not in rats given LPS (100 μg/kg) on postnatal day 10. Expression of hypothalamic IL-1β and TNF-α mRNA, which suppress serum LH during immune stress, were equally increased in these groups by adult LPS (400 μg/kg) injection. The present data suggest that the period prior to postnatal day 10 is the critical window in which immune stress can induce long-lasting alterations in the LH response, but that IL-1β and TNF-α are not involved in mediating the altered response.
authors.affiliation: Department of Obstetrics and Gynecology, The University of Tokushima Graduate School, Institute of Health Biosciences, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan.
authors.forename: Takeshi
authors.initials: T
authors.lastname: Iwasa
authors.forename: Toshiya
authors.initials: T
authors.lastname: Matsuzaki
authors.forename: Masahiro
authors.initials: M
authors.lastname: Murakami
authors.forename: Riyo
authors.initials: R
authors.lastname: Kinouchi
authors.forename: Ganbat
authors.initials: G
authors.lastname: Gereltsetseg
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Nakazawa
authors.forename: Satoshi
authors.initials: S
authors.lastname: Yamamoto
authors.forename: Akira
authors.initials: A
authors.lastname: Kuwahara
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Yasui
authors.forename: Minoru
authors.initials: M
authors.lastname: Irahara
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D004781:Environmental Exposure / Q000009:adverse effects; D005260:Female; D018507:Gene Expression Regulation, Developmental / Q000276:immunology; D007031:Hypothalamus / Q000276:immunology*; D007107:Immune System / Q000254:growth & development / Q000502:physiology*; D053583:Interleukin-1beta / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D008070:Lipopolysaccharides / Q000008:administration & dosage; D007986:Luteinizing Hormone / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D008297:Male; D015213:Neuroimmunomodulation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012098:Reproduction / Q000276:immunology; D013312:Stress, Physiological / Q000276:immunology*; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000276:immunology / Q000378:metabolism
chemical_list: D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D007986:Luteinizing Hormone