title: Autoantibodies to IL-1 alpha in sera from rapidly progressive idiopathic pulmonary fibrosis.
abstract: To clarify the clinical significance of autoantibodies to interleukin-1 alpha (IL-1 alpha autoantibodies) in rapidly progressive idiopathic pulmonary fibrosis (IPF), we measured the level of IL-1 alpha autoantibodies in serum of 11 patients on the first hospital day, when patients were admitted due to severe symptoms, and on the 21st hospital day. IL-1 alpha autoantibodies in serum were measured using radioimmunoassay, and the limitation of this assay for IL-1 alpha autoantibodies was 5 ng/ml. These antibodies were detected in 5 of 11 patients on the first hospital day. On the 21st hospital day, these antibodies were detected in all patients, and its level was increased compared with that on the first hospital day. IL-1 alpha autoantibodies that appeared in patients corresponded to that of IgG. The half life of exogenous autoantibodies was investigated following administration of autoantibody rich plasma obtained from healthy blood donors to 6 control patients (CP) and 6 progressive IPF patients. These autoantibody levels in their serum were less than 5 ng/ml before administration. Serum was obtained at the indicated time after administration of IL-1 alpha autoantibodies and the level of these autoantibodies in serum was measured, then the half life was calculated. Half life of exogenous IL-1 alpha autoantibodies in progressive IPF patients was significantly shorter than that in CP (71.3 +/- 31.8 hr vs 352.0 +/- 98.3 hr, p < 0.01). These findings suggested that IL-1 alpha autoantibodies were generated in response to the inflammatory process of rapidly progressive IPF and may act as a regulatory factor for IL-1 alpha.
authors.affiliation: Third Department of Internal Medicine, University Hospital, University of Tokushima School of Medicine, Tokushima, Japan.
authors.forename: F
authors.initials: F
authors.lastname: Ogushi
authors.forename: K
authors.initials: K
authors.lastname: Tani
authors.forename: T
authors.initials: T
authors.lastname: Endo
authors.forename: H
authors.initials: H
authors.lastname: Tada
authors.forename: T
authors.initials: T
authors.lastname: Kawano
authors.forename: T
authors.initials: T
authors.lastname: Asano
authors.forename: L
authors.initials: L
authors.lastname: Huang
authors.forename: Y
authors.initials: Y
authors.lastname: Ohmoto
authors.forename: M
authors.initials: M
authors.lastname: Muraguchi
authors.forename: H
authors.initials: H
authors.lastname: Moriguchi
authors.forename: S
authors.initials: S
authors.lastname: Sone
mesh_terms: D000368:Aged; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D001323:Autoantibodies / Q000097:blood / Q000276:immunology*; D001324:Autoantigens / Q000276:immunology*; D018450:Disease Progression; D004417:Dyspnea / Q000209:etiology; D005260:Female; D006207:Half-Life; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007375:Interleukin-1 / Q000276:immunology*; D008297:Male; D008775:Methylprednisolone / Q000627:therapeutic use; D008875:Middle Aged; D011239:Prednisolone / Q000627:therapeutic use; D011658:Pulmonary Fibrosis / Q000097:blood / Q000150:complications / Q000188:drug therapy / Q000276:immunology*; D012907:Smoking; D016896:Treatment Outcome
chemical_list: D000893:Anti-Inflammatory Agents; D001323:Autoantibodies; D001324:Autoantigens; D007166:Immunosuppressive Agents; D007375:Interleukin-1; D011239:Prednisolone; D008775:Methylprednisolone