title: Interleukin 6, but not ciliary neurotrophic factor or leukaemia inhibitory factor, is responsible for the acute phase response to turpentine-induced myositis.
abstract: The acute phase response to inflammation is mediated in part by the endogenous production of pro-inflammatory cytokines. Interleukin 6 (IL-6) and members of its superfamily, including ciliary neurotrophic factor (CNTF) and leukaemia inhibitory factor (LIF) have been implicated as primary mediators of the hepatic acute phase response. In the present report, mice suffering a turpentine-induced myositis were passively immunized with antibodies against either IL-6, CNTF or LIF. Passive immunization against IL-6 attenuated the anorexia and completely prevented the hypoalbuminaemia, and increases in the serum concentration of the acute phase reactants, amyloid P, amyloid A and seromucoid. In contrast, passive immunization against either CNTF or LIF failed to modulate the anorexia, weight loss or hepatic acute phase protein responses. The findings suggest that IL-6, but not other members of its superfamily, is primarily responsible for the hepatic acute phase response, and contributes to the anorexia, associated with turpentine-induced myositis.
authors.affiliation: Department of Surgery, University of Florida College of Medicine, Gainesville, FL 32610, USA.
authors.forename: A
authors.initials: A
authors.lastname: Kaibara
authors.forename: N J
authors.initials: NJ
authors.lastname: Espat
authors.forename: T
authors.initials: T
authors.lastname: Auffenberg
authors.forename: A S
authors.initials: AS
authors.lastname: Abouhamze
authors.forename: D
authors.initials: D
authors.lastname: Martin
authors.forename: S
authors.initials: S
authors.lastname: Kalra
authors.forename: L L
authors.initials: LL
authors.lastname: Moldawer
mesh_terms: D000210:Acute-Phase Reaction / Q000503:physiopathology*; D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D001835:Body Weight / Q000187:drug effects; D020934:Ciliary Neurotrophic Factor; D004435:Eating / Q000187:drug effects; D005260:Female; D006131:Growth Inhibitors / Q000276:immunology / Q000502:physiology*; D007116:Immunization, Passive; D015850:Interleukin-6 / Q000276:immunology / Q000502:physiology*; D053605:Leukemia Inhibitory Factor; D008222:Lymphokines / Q000276:immunology / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D009220:Myositis / Q000139:chemically induced / Q000276:immunology*; D009419:Nerve Tissue Proteins / Q000276:immunology / Q000502:physiology*; D009961:Orosomucoid / Q000032:analysis; D012709:Serum Albumin / Q000032:analysis; D000685:Serum Amyloid A Protein / Q000032:analysis; D000683:Serum Amyloid P-Component / Q000032:analysis; D014425:Turpentine
chemical_list: D000911:Antibodies, Monoclonal; D020934:Ciliary Neurotrophic Factor; D006131:Growth Inhibitors; D015850:Interleukin-6; D053605:Leukemia Inhibitory Factor; C507838:Lif protein, mouse; D008222:Lymphokines; D009419:Nerve Tissue Proteins; D009961:Orosomucoid; D012709:Serum Albumin; D000685:Serum Amyloid A Protein; D000683:Serum Amyloid P-Component; D014425:Turpentine