title: Normal aging of offspring mice of mothers with induced inflammation during pregnancy.
abstract: Intrauterine inflammation is a major risk for offspring neurodevelopmental brain damage and may result in cognitive limitations and poor cognitive and perceptual outcomes. In the present study we tested the possibility that prenatal exposure to a high level of inflammatory factors may increase the risk for neurodegeneration in aging. The effect of systemic maternal inflammation (MI), induced by lipopolysaccharide (LPS) on offspring brain aging, was examined in 8 month old (adult) and 20 month old (aged) offspring mice. A significant effect of age was found in the distance and velocity of exploration in the open field in both groups. In addition, MI aged offspring covered longer distances and enter frequently to the center of the field compared with the aged control group. Although only little difference was found in the aged MI offspring compared with the control offspring, the overall profile of behavior of these mice differs from that of the control group, as detected by clustering analysis. The expression of the death-associated protein FAS-ligand and the amount of apoptotic cell death were examined in the brains of aged offspring. Similar levels of FAS-ligand expression and parallel density of apoptotic cells were detected in the brains of aged mice of control and MI groups. Altogether, moderate systemic MI was not found to increase the risk for cell death in the aged offspring; limited effect was found in mice profile of behavior.
authors.affiliation: Department of Developmental Molecular Genetics and Zlotowski Center for Neuroscience, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel 84105. havag@bgu.ac.il
authors.forename: H
authors.initials: H
authors.lastname: Golan
authors.forename: M
authors.initials: M
authors.lastname: Stilman
authors.forename: V
authors.initials: V
authors.lastname: Lev
authors.forename: M
authors.initials: M
authors.lastname: Huleihel
mesh_terms: D000367:Age Factors; D000375:Aging / Q000187:drug effects / Q000502:physiology*; D000704:Analysis of Variance; D000818:Animals; D000831:Animals, Newborn; D001522:Behavior, Animal; D001921:Brain / Q000187:drug effects / Q000254:growth & development / Q000473:pathology; D016923:Cell Death / Q000502:physiology; D016207:Cytokines / Q000378:metabolism; D005106:Exploratory Behavior; D053222:Fas Ligand Protein / Q000378:metabolism; D005260:Female; D005865:Gestational Age; D007150:Immunohistochemistry / Q000379:methods; D007249:Inflammation / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D007858:Learning / Q000502:physiology; D008070:Lipopolysaccharides / Q000633:toxicity; D051379:Mice; D009043:Motor Activity / Q000187:drug effects / Q000502:physiology; D011247:Pregnancy; D011248:Pregnancy Complications; D011297:Prenatal Exposure Delayed Effects
chemical_list: D016207:Cytokines; D053222:Fas Ligand Protein; D008070:Lipopolysaccharides