title: Central interleukin-10 attenuates lipopolysaccharide-induced changes in food intake, energy expenditure and hypothalamic Fos expression.
abstract: Lipopolysaccharide (LPS) is often used to mimic acute infection and induces hypophagia, the selective partitioning of fat for energy, and fever. Interleukin-10 (IL-10) is an anti-inflammatory cytokine expressed in the brain which attenuates LPS-induced hypophagia; however the potential sites of interaction within the brain have not been investigated. Hypothalamic orexin (ORX) and melanin-concentrating hormone (MCH) regulate energy expenditure and food intake although the regulation of these neuropeptides through the interactions between central IL-10 and the inflammatory consequences of peripheral LPS have not been investigated. The present study in the rat investigated during the dark phase of the light-dark cycle the ability of central IL-10 (250 ng, i.c.v.) to attenuate the changes in food intake, energy substrate partitioning, and central Fos expression within the hypothalamus to peripheral LPS (100 microg/kg, i.p.); Fos expression changes specifically within ORX and MCH neurons were also investigated. Central IL-10 attenuated the peripheral LPS-induced hypophagia, reduction in motor activity, fever and reduction in respiratory exchange ratio. Central IL-10 also attenuated peripheral LPS-induced increases in Fos expression within ORX neurons and decreases in Fos expression within unidentified cells of the caudal arcuate nucleus. In contrast, both IL-10 and LPS injection independently decreased Fos expression within MCH neurons. The present study provides further insight into the interactions within the brain between the anti-inflammatory cytokine IL-10, the inflammatory consequences of LPS, and neuropeptides known to regulate energy expenditure and food intake.
authors.affiliation: Department of Physiology, Monash University, Victoria, Australia. jacob.hollis@med.monash.edu.au
authors.forename: Jacob H
authors.initials: JH
authors.lastname: Hollis
authors.forename: Moyra
authors.initials: M
authors.lastname: Lemus
authors.forename: Megan J
authors.initials: MJ
authors.lastname: Evetts
authors.forename: Brian J
authors.initials: BJ
authors.lastname: Oldfield
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000633:toxicity; D004435:Eating / Q000187:drug effects / Q000502:physiology*; D004734:Energy Metabolism / Q000187:drug effects / Q000502:physiology*; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology; D007031:Hypothalamus / Q000187:drug effects / Q000378:metabolism*; D018836:Inflammation Mediators / Q000008:administration & dosage / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000633:toxicity; D007276:Injections, Intraventricular; D016753:Interleukin-10 / Q000008:administration & dosage*; D008070:Lipopolysaccharides / Q000037:antagonists & inhibitors* / Q000633:toxicity*; D008297:Male; D009479:Neuropeptides / Q000502:physiology; D016760:Proto-Oncogene Proteins c-fos / Q000096:biosynthesis*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011994:Recombinant Proteins / Q000008:administration & dosage
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D009479:Neuropeptides; D016760:Proto-Oncogene Proteins c-fos; D011994:Recombinant Proteins; D016753:Interleukin-10