title: The conditioned enhancement of neutrophil activity is catecholamine dependent.
abstract: Neutrophil activity was elevated in the conditioned mice for the first time through an established conditioned training process. Catecholamines were proved to be important in the regulation of this conditioned innate immunity. In the study, the camphor odor (as the conditioned stimulus, CS) and poly I: C (as the unconditioned stimulus, US) was used to conditionally elevate the activity of the splenic neutrophils. The mechanism(s) responsible for the conditioned enhancement of neutrophil activity was further investigated using the neurochemical blocking assay and immunohistochemical analysis. Results showed that the neutrophil activity was significantly enhanced through the conditioned training process; both reserpine and 6-hydroxydopamine (6-OHDA) significantly blocked this conditioned innate immunity at the conditioned recall stage. Dexamethasone (Dex), however, showed no effect on the conditioned neutrophil response. Tyrosine hydroxylase (TH)-positive cells significantly increased in the locus coeruleus (LC), hypothalamus, and cortex but not in the spleen of the conditioned animals. These results indicate that during the conditioned recall stage, the brain signals the splenic neutrophils via the sympathetic nervous system (SNS) by releasing the peripheral catecholamines in spleen. The activation of the SNS, on the other hand, is also under the influence of catecholamines released in the LC. The hypothalamic pituitary (HP) axis, on the other hand, plays no role in the regulation of the conditioned neutrophil response.
authors.affiliation: Department of Life Sciences, National Chung-Hsing University, Taichung, 40227, Taiwan.
authors.forename: Hsin-Ju
authors.initials: HJ
authors.lastname: Chao
authors.forename: Yung-Chang
authors.initials: YC
authors.lastname: Hsu
authors.forename: Hui-Ping
authors.initials: HP
authors.lastname: Yuan
authors.forename: Haung-Shiang
authors.initials: HS
authors.lastname: Jiang
authors.forename: Chi-Mei
authors.initials: CM
authors.lastname: Hsueh
mesh_terms: D018663:Adrenergic Agents / Q000494:pharmacology; D018759:Adrenergic Uptake Inhibitors / Q000494:pharmacology; D000704:Analysis of Variance; D000818:Animals; D000891:Anti-Infective Agents, Local / Q000494:pharmacology; D001522:Behavior, Animal / Q000502:physiology; D001921:Brain / Q000033:anatomy & histology / Q000187:drug effects / Q000378:metabolism; D001923:Brain Chemistry / Q000187:drug effects / Q000502:physiology; D002164:Camphor / Q000494:pharmacology; D002395:Catecholamines / Q000502:physiology*; D002448:Cell Adhesion / Q000187:drug effects; D002452:Cell Count; D003213:Conditioning, Psychological / Q000502:physiology*; D005260:Female; D007150:Immunohistochemistry / Q000379:methods; D007369:Interferon Inducers / Q000494:pharmacology; D051379:Mice; D008807:Mice, Inbred BALB C; D009504:Neutrophils / Q000187:drug effects / Q000502:physiology*; D009573:Nitrites / Q000378:metabolism; D016627:Oxidopamine / Q000494:pharmacology; D009195:Peroxidase / Q000378:metabolism; D011070:Poly I-C / Q000494:pharmacology; D012110:Reserpine / Q000494:pharmacology; D013154:Spleen / Q000166:cytology* / Q000378:metabolism; D013997:Time Factors; D014343:Trypan Blue; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
chemical_list: D018663:Adrenergic Agents; D018759:Adrenergic Uptake Inhibitors; D000891:Anti-Infective Agents, Local; D002395:Catecholamines; D007369:Interferon Inducers; D009573:Nitrites; D002164:Camphor; D012110:Reserpine; D016627:Oxidopamine; D009195:Peroxidase; D014446:Tyrosine 3-Monooxygenase; D014343:Trypan Blue; D011070:Poly I-C