title: Allergic fetal priming leads to developmental, behavioral and neurobiological changes in mice.
abstract: The state of the mother's immune system during pregnancy has an important role in fetal development and disruptions in the balance of this system are associated with a range of neurologic, neuropsychiatric and neurodevelopmental disorders. Epidemiological and clinical reports reveal various clues that suggest a possible association between developmental neuropsychiatric disorders and family history of immune system dysfunction. Over the past three decades, analogous increases have been reported in both the incidence of neurodevelopmental disorders and immune-related disorders, particularly allergy and asthma, raising the question of whether allergic asthma and characteristics of various neurodevelopmental disorders share common causal links. We used a mouse model of maternal allergic asthma to test this novel hypothesis that early fetal priming with an allergenic exposure during gestation produces behavioral deficits in offspring. Mothers were primed with an exposure to ovalbumin (OVA) before pregnancy, then exposed to either aerosolized OVA or vehicle during gestation. Both male and female mice born to mothers exposed to aerosolized OVA during gestation exhibited altered developmental trajectories in weight and length, decreased sociability and increased marble-burying behavior. Moreover, offspring of OVA-exposed mothers were observed to have increased serotonin transporter protein levels in the cortex. These data demonstrate that behavioral and neurobiological effects can be elicited following early fetal priming with maternal allergic asthma and provide support that maternal allergic asthma may, in some cases, be a contributing factor to neurodevelopmental disorders.
authors: Program in Neuroscience and Behavior, Department of Psychology and Education, Mount Holyoke College, South Hadley, MA, USA.
authors: J J
authors: JJ
authors: Schwartzer
authors: Department of Medical Microbiology and Immunology, University of California, Davis, Davis, CA, USA.
authors: M
authors: M
authors: Careaga
authors: Department of Medical Microbiology and Immunology, University of California, Davis, Davis, CA, USA.
authors: C
authors: C
authors: Chang
authors: Department of Medical Microbiology and Immunology, University of California, Davis, Davis, CA, USA.
authors: C E
authors: CE
authors: Onore
authors: Department of Medical Microbiology and Immunology, University of California, Davis, Davis, CA, USA.
authors: P
authors: P
authors: Ashwood
mesh_terms: D000818:Animals; D001249:Asthma / Q000276:immunology* / Q000503:physiopathology; D001522:Behavior, Animal; D015153:Blotting, Western; D002540:Cerebral Cortex / Q000378:metabolism*; D004195:Disease Models, Animal; D005260:Female; D006130:Growth Disorders / Q000276:immunology* / Q000503:physiopathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009035:Mothers; D010047:Ovalbumin / Q000008:administration & dosage; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000276:immunology* / Q000503:physiopathology; D050486:Serotonin Plasma Membrane Transport Proteins / Q000378:metabolism
chemical_list: D050486:Serotonin Plasma Membrane Transport Proteins; C493231:Slc6a4 protein, mouse; D010047:Ovalbumin