title: Parental experience of a risky environment leads to improved offspring growth rate.
abstract: Parasites (or diseases) are a major selective force for the evolution of life history traits and parasite-host evolution. Mothers can show a variety of responses to parasites during pregnancy, with different consequences for them or their offspring. However, whether information in the maternal environment before pregnancy can cause a change in the phenotype of the offspring is unknown. To avoid the confounding effect of pathogens and to reduce the risk of a direct effect of maternal immune system activation, we injected female laboratory mice with lipopolysaccharides (LPS) before they mated. In order to provide constant information on the potential infectious risk of the environment, females were mated with males that were also exposed to LPS before mating. Offspring from immune-challenged parents were larger and grew at a faster rate than offspring from control parents (injected with PBS). Additionally, offspring from immune-challenged parents that suffered the most from inflammation grew at a faster rate than offspring from low suffering parents. Producing heavier offspring that will reach sexual maturity earlier is likely to have fitness benefits for parents and offspring through improved reproductive success.
authors.affiliation: Biogéosciences, UMR 6282, CNRS, Université de Bourgogne, 21000 Dijon, France Department of Zoology, University of Otago, PO Box 56, Dunedin 9054, New Zealand anne.besson@gmail.com.
authors.forename: Anne A
authors.initials: AA
authors.lastname: Besson
authors.affiliation: Biogéosciences, UMR 6282, CNRS, Université de Bourgogne, 21000 Dijon, France.
authors.forename: Romain
authors.initials: R
authors.lastname: Guerreiro
authors.affiliation: Physiopathologie des Dyslipidémies, UMR U866, INSRM, Université de Bourgogne, 21000 Dijon, France.
authors.forename: Jérôme
authors.initials: J
authors.lastname: Bellenger
authors.affiliation: Biochimie Métabolique et Nutritionnelle, UMR U866, INSRM, Université de Bourgogne, 21000 Dijon, France.
authors.forename: Kevin
authors.initials: K
authors.lastname: Ragot
authors.affiliation: Biogéosciences, UMR 6282, CNRS, Université de Bourgogne, 21000 Dijon, France.
authors.forename: Bruno
authors.initials: B
authors.lastname: Faivre
authors.affiliation: Biogéosciences, UMR 6282, CNRS, Université de Bourgogne, 21000 Dijon, France.
authors.forename: Gabriele
authors.initials: G
authors.lastname: Sorci
mesh_terms: D000818:Animals; D049628:Body Size / Q000502:physiology; D005260:Female; D007107:Immune System / Q000502:physiology; D007249:Inflammation / Q000503:physiopathology; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D018811:Maternal Exposure; D051379:Mice / Q000254:growth & development* / Q000276:immunology*; D018812:Paternal Exposure; D011247:Pregnancy
chemical_list: D008070:Lipopolysaccharides
keywords: Fetal programming; Inflammation; Maternal effect; Rodent; Thrifty gene hypothesis