title: Exaggerated messenger RNA expression of inflammatory cytokines in human T-cell lymphotropic virus type I-associated myelopathy.
abstract: OBJECTIVE
  To investigate the expression of inflammatory cytokine messenger RNA (mRNA) in peripheral blood mononuclear cells of patients with human T-cell lymphotropic virus type I (HTLV-I)-associated myelopathy (HAM).
  
  
  METHODS
  Seventeen patients with HAM, 18 HTLV-I-seropositive carriers, and 10 seronegative individuals were studied.
  
  
  METHODS
  We compared the expression of tumor necrosis factor alpha (TNF-alpha), granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon alpha (IFN-alpha), IFN-beta, and IFN-gamma, and interleukin 1 alpha (IL-1 alpha) and IL-1 beta by reverse transcriptase-polymerase chain reaction.
  
  
  RESULTS
  In patients with HAM, the reverse transcriptase-polymerase chain reaction products of TNF-alpha, GM-CSF, IFN-gamma, and IL-1 alpha were detected in significantly higher incidences than in HTLV-I-seropositive carriers and seronegative controls. Furthermore, simultaneous mRNA expression of three or more of these four cytokines was detected in all patients with HAM compared with only 21.4% of HTLV-I-seropositive carriers. By contrast, there was no significant difference in mRNA expression of IFN-alpha, IFN-beta, and IL-1 beta among patients with HAM, HTLV-I-seropositive carriers, and HTLV-I-seronegative controls.
  
  
  CONCLUSIONS
  An exaggerated mRNA expression of several inflammatory cytokines, including TNF-alpha, GM-CSF, IFN-gamma, and IL-1 alpha, was demonstrated in peripheral blood mononuclear cells of patients with HAM. Moreover, transcripts of these cytokines were simultaneously up-regulated in patients with HAM, suggesting that an inflammatory state in the central nervous system may be related to the pathogenesis of HAM.
authors.affiliation: First Department of Internal Medicine, Nagasaki, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Watanabe
authors.forename: T
authors.initials: T
authors.lastname: Nakamura
authors.forename: K
authors.initials: K
authors.lastname: Nagasato
authors.forename: S
authors.initials: S
authors.lastname: Shirabe
authors.forename: K
authors.initials: K
authors.lastname: Ohishi
authors.forename: K
authors.initials: K
authors.lastname: Ichinose
authors.forename: Y
authors.initials: Y
authors.lastname: Nishiura
authors.forename: S
authors.initials: S
authors.lastname: Chiyoda
authors.forename: M
authors.initials: M
authors.lastname: Tsujihata
authors.forename: S
authors.initials: S
authors.lastname: Nagataki
mesh_terms: D000328:Adult; D000368:Aged; D001483:Base Sequence; D016207:Cytokines / Q000235:genetics*; D005260:Female; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000235:genetics; D006801:Humans; D016898:Interferon-alpha / Q000235:genetics; D016899:Interferon-beta / Q000235:genetics; D007371:Interferon-gamma / Q000235:genetics; D007375:Interleukin-1 / Q000235:genetics; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D015493:Paraparesis, Tropical Spastic / Q000235:genetics*; D012333:RNA, Messenger / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D016207:Cytokines; D016898:Interferon-alpha; D007375:Interleukin-1; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D016899:Interferon-beta; D007371:Interferon-gamma; D016178:Granulocyte-Macrophage Colony-Stimulating Factor