title: Interleukin-6 increases intracellular Ca2+ concentration and induces catecholamine secretion in rat carotid body glomus cells.
abstract: Although abundant evidence indicates mutual regulation between the immune and the central nervous systems, how the immune signals are transmitted to the brain is still an unresolved question. In a previous study we found strong expression of proinflammatory cytokine receptors, including interleukin (IL)-1 receptor I and IL-6 receptor alpha in the rat carotid body (CB), a well-known arterial chemoreceptor that senses a variety of chemostimuli in the arterial blood. We demonstrated that IL-1 stimulation increases intracellular calcium ([Ca(2+)](i)) in CB glomus cells, releases ATP, and increases the discharge rate in carotid sinus nerve. To explore the effect of IL-6 on CB, here we examine the effect of IL-6 on [Ca(2+)](i) and catecholamine (CA) secretion in rat CB glomus cells. Calcium imaging showed that extracellular application of IL-6 induced a rise in [Ca(2+)](i) in cultured glomus cells. Amperometry showed that local application of IL-6 evoked CA release from glomus cells. Furthermore, the CA secretory response to IL-6 was blocked by 200 microM Cd(2+), a well-known Ca(2+) channel blocker. Our experiments provide further evidence for the responsiveness of the CB to proinflammatory cytokines and indicate that the CB might play a role in inflammation sensing and transmission of such information to the brain.
authors.affiliation: Institute of Neurosciences, Fourth Military Medical University, Xi'an, Shaanxi, China.
authors.forename: Juan
authors.initials: J
authors.lastname: Fan
authors.forename: Bo
authors.initials: B
authors.lastname: Zhang
authors.forename: Hai-Feng
authors.initials: HF
authors.lastname: Shu
authors.forename: Xiao-Yu
authors.initials: XY
authors.lastname: Zhang
authors.forename: Xi
authors.initials: X
authors.lastname: Wang
authors.forename: Fang
authors.initials: F
authors.lastname: Kuang
authors.forename: Ling
authors.initials: L
authors.lastname: Liu
authors.forename: Zheng-Wu
authors.initials: ZW
authors.lastname: Peng
authors.forename: Rui
authors.initials: R
authors.lastname: Wu
authors.forename: Zhuan
authors.initials: Z
authors.lastname: Zhou
authors.forename: Bai-Ren
authors.initials: BR
authors.lastname: Wang
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002104:Cadmium / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling / Q000187:drug effects / Q000502:physiology; D002344:Carotid Body / Q000187:drug effects / Q000378:metabolism*; D002395:Catecholamines / Q000378:metabolism*; D002628:Chemoreceptor Cells / Q000187:drug effects / Q000378:metabolism*; D007375:Interleukin-1 / Q000378:metabolism / Q000494:pharmacology; D015850:Interleukin-6 / Q000378:metabolism* / Q000494:pharmacology; D007424:Intracellular Fluid / Q000378:metabolism; D008297:Male; D015213:Neuroimmunomodulation / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017472:Receptors, Interleukin-1 / Q000187:drug effects / Q000378:metabolism; D019947:Receptors, Interleukin-6 / Q000187:drug effects / Q000378:metabolism; D015854:Up-Regulation / Q000187:drug effects / Q000502:physiology
chemical_list: D002395:Catecholamines; D007375:Interleukin-1; D015850:Interleukin-6; D017472:Receptors, Interleukin-1; D019947:Receptors, Interleukin-6; D002104:Cadmium; D000255:Adenosine Triphosphate; D002118:Calcium