title: Social interactions alter proinflammatory cytokine gene expression and behavior following endotoxin administration.
abstract: Sick animals display a constellation of behaviors, including anhedonia, anorexia, and reduced social interactions. Acute infection eliminates female mating behavior, but fails to attenuate mating behavior in male rats. These results have been attributed to the different reproductive strategies and parental investment of the two sexes. Males putatively suppress the symptoms of infection in order to "deceive" females into mating. We sought to investigate the mechanisms responsible for this suppression. Adult male CD-1 mice were treated with lipopolysaccharide (LPS; a component of bacterial cell walls; 400 microg/kg), then paired 2 h later with a receptive female or juvenile male or remained isolated. Blood samples and brains of the males were collected 3 h post-LPS; hypothalamic interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNFalpha) gene expression was measured using RT-PCR. Contrary to our prediction, exposure to a female increased hypothalamic IL-1 and TNFalpha gene expression. LPS treatment significantly decreased testosterone and increased corticosterone secretions. Social interactions altered absolute corticosterone concentrations in saline-injected animals only. In order to determine whether increased production of hypothalamic cytokines reflected increased severity of sickness responses, body temperature was monitored in a second group of mice implanted with telemetric transmitters. Body mass, food intake, and consumption of sweetened condensed milk (a highly favored food) were also monitored in these mice for 72 h post-injection. LPS injections reduced milk intake, an effect that was modulated by social interactions; however, fever was unaltered relative to isolated animals. These results suggest that social interactions can adjust behavioral responses to infection although the ultimate cause of this adjustment remains unspecified.
authors.affiliation: Department of Neuroscience, Institute for Behavioral Medicine Research, The Ohio State University, Columbus, OH 43210, USA. weil.20@osu.edu
authors.forename: Zachary M
authors.initials: ZM
authors.lastname: Weil
authors.forename: Stephanie L
authors.initials: SL
authors.lastname: Bowers
authors.forename: Leah M
authors.initials: LM
authors.lastname: Pyter
authors.forename: Randy J
authors.initials: RJ
authors.lastname: Nelson
mesh_terms: D000367:Age Factors; D000704:Analysis of Variance; D000818:Animals; D001424:Bacterial Infections / Q000139:chemically induced / Q000503:physiopathology / Q000523:psychology; D003345:Corticosterone / Q000097:blood; D016207:Cytokines; D005247:Feeding Behavior / Q000502:physiology; D005260:Female; D005786:Gene Expression Regulation / Q000276:immunology; D007031:Hypothalamus / Q000378:metabolism*; D007375:Interleukin-1 / Q000235:genetics / Q000378:metabolism*; D008070:Lipopolysaccharides; D008297:Male; D051379:Mice; D012313:RNA / Q000032:analysis; D011897:Random Allocation; D012803:Sick Role; D012919:Social Behavior; D018709:Statistics, Nonparametric; D013739:Testosterone / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism*
chemical_list: D016207:Cytokines; D007375:Interleukin-1; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D013739:Testosterone; D012313:RNA; D003345:Corticosterone