title: Lateralization and catecholaminergic neuroimmunomodulation: prazosin, an alpha1/alpha2-adrenergic receptor antagonist, suppresses interleukin-1 and increases interleukin-10 production induced by lipopolysaccharides.
abstract: OBJECTIVE
  The brain has previously been shown to asymmetrically modulate neurochemical, neuroendocrine and immune responses to lipopolysaccharides (LPS). As these responses are reversed by a chemical sympathectomy, it can be hypothesized that the asymmetry in the functioning of the sympathetic nervous system may be one of the mechanisms by which the brain hemispheres asymmetrically modulate immune reactivity.
  
  
  METHODS
  The effects of prazosin, an alpha1/alpha2-adrenergic receptor antagonist, on the production of interleukin (IL)-1beta and IL-10 induced by LPS was studied in mice selected for their paw preference.
  
  
  RESULTS
  Two hours after intraperitoneal injection of 5 microg of LPS, plasma levels of IL-1beta were higher in right-pawed mice as compared to left-pawed or ambidextrous animals. No lateralization effect was observed for LPS-induced plasma IL-10 levels. Prazosin, 10 mg/kg, injected intraperitoneally half an hour before LPS, reduced plasma levels of IL-1beta and abolished the effect of lateralization. By contrast, prazosin drastically increased plasma levels of IL-10 in response to LPS and the production of corticosterone in untreated controls.
  
  
  CONCLUSIONS
  These results suggest that the catecholaminergic modulation of immune reactivity depends on lateralization. This work further demonstrates that prazosin is endowed with anti-inflammatory properties that may be considered side effects of this drug, which is widely prescribed in the treatment of hypertension.
authors.affiliation: Neurobiologie Intégrative U394, Institut François Magendie, Bordeaux, France.
authors.forename: Jing
authors.initials: J
authors.lastname: Dong
authors.forename: Oulaya
authors.initials: O
authors.lastname: Mrabet
authors.forename: Elisabeth
authors.initials: E
authors.lastname: Moze
authors.forename: KangSheng
authors.initials: K
authors.lastname: Li
authors.forename: Pierre J
authors.initials: PJ
authors.lastname: Neveu
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D001921:Brain / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D002395:Catecholamines / Q000276:immunology* / Q000378:metabolism; D002478:Cells, Cultured; D003345:Corticosterone / Q000097:blood; D005260:Female; D007839:Functional Laterality / Q000187:drug effects / Q000502:physiology*; D007375:Interleukin-1 / Q000097:blood / Q000378:metabolism; D016753:Interleukin-10 / Q000097:blood / Q000378:metabolism; D007378:Interleukins / Q000378:metabolism*; D051379:Mice; D008809:Mice, Inbred C3H; D009434:Neural Pathways / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D015213:Neuroimmunomodulation / Q000187:drug effects / Q000502:physiology*; D011224:Prazosin / Q000494:pharmacology*; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism
chemical_list: D000317:Adrenergic alpha-Antagonists; D000893:Anti-Inflammatory Agents; D002395:Catecholamines; D007375:Interleukin-1; D007378:Interleukins; D016753:Interleukin-10; D003345:Corticosterone; D011224:Prazosin