title: Circulating transforming growth factor beta 1 (TGF-beta1) in Guillain-Barré syndrome: decreased concentrations in the early course and increase with motor function.
abstract: OBJECTIVE
  To delineate the possible implication of the immunosuppressive cytokine transforming growth factor beta 1 (TGF-beta1) in the pathogenesis of Guillain-Barré syndrome. Guillain-Barré syndrome is a disorder that may implicate cytokines in its pathogenesis. TGF-beta1 is a potent anti-inflammatory cytokine occasionally shown to be regulated in the course of demyelinating disorders.
  
  
  METHODS
  The study measured circulating proinflammatory and anti-inflammatory cytokines from the progressing phase to early recovery in patients with Guillain-Barré syndrome. Plasma concentrations of TNF-alpha, IL-beta1, IL-2, IL-4, IL-6, IL-10, and TGF-beta1 were prospectively evaluated in 15 patients with Guillain-Barré syndrome every three days for the first 15 days after admission to hospital, and in 15 controls with non-inflammatory neurological diseases.
  
  
  RESULTS
  Concentrations of TGF-beta1 in plasma were decreased in 13115 patients (87 %) at day 1, remained low during progression and the plateau of paralysis (days 1-10), and then progressively increased up to control concentrations during early recovery (days 12-15). Concentrations of plasma TGF-beta1 correlated positively with motor function, the lowest values being e found in the most disabled patients. Concentrations of plasma TGF-beta1 were decreased before any treatment, and during treatment by either plasma exchange or intravenous immunoglobulins, plasma exchange being associated with a more pronounced decrease in TGF-beta1 at day 7. Circulating TNF-alpha concentrations were raised, as previously reported, when other cytokines were either randomly increased (IL-2, IL-6), or undetectable (IL-1, IL-4, IL-7, IL-10).
  
  
  CONCLUSIONS
  Down regulation of TGF-beta1 in the early course of Guillain-Barré syndrome could participate in neural inflammation.
authors.affiliation: Réseau de Neuroimmunologie du Nerf Périphérique (AP/HP), Créteil, France.
authors.forename: A
authors.initials: A
authors.lastname: Créange
authors.forename: L
authors.initials: L
authors.lastname: Bélec
authors.forename: B
authors.initials: B
authors.lastname: Clair
authors.forename: J D
authors.initials: JD
authors.lastname: Degos
authors.forename: J C
authors.initials: JC
authors.lastname: Raphaël
authors.forename: R K
authors.initials: RK
authors.lastname: Gherardi
mesh_terms: D000276:Adjuvants, Immunologic / Q000627:therapeutic use*; D002465:Cell Movement / Q000502:physiology*; D018450:Disease Progression; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D016756:Immunoglobulins, Intravenous / Q000627:therapeutic use; D010950:Plasma Cells / Q000502:physiology*; D010951:Plasma Exchange / Q000379:methods; D011129:Polyradiculoneuropathy / Q000097:blood* / Q000150:complications* / Q000628:therapy; D011446:Prospective Studies; D011596:Psychomotor Disorders / Q000175:diagnosis / Q000209:etiology*; D012720:Severity of Illness Index; D013997:Time Factors; D016211:Transforming Growth Factor alpha / Q000097:blood / Q000378:metabolism; D016212:Transforming Growth Factor beta / Q000097:blood* / Q000378:metabolism*; D000511:alpha-Macroglobulins / Q000378:metabolism*
chemical_list: D000276:Adjuvants, Immunologic; D016756:Immunoglobulins, Intravenous; D016211:Transforming Growth Factor alpha; D016212:Transforming Growth Factor beta; D000511:alpha-Macroglobulins; D006854:Hydrocortisone