EXAGGERATED MESSENGER-RNA EXPRESSION OF INFLAMMATORY CYTOKINES IN HUMAN T-CELL LYMPHOTROPIC VIRUS TYPE I-ASSOCIATED MYELOPATHY

Citation
H. Watanabe et al., EXAGGERATED MESSENGER-RNA EXPRESSION OF INFLAMMATORY CYTOKINES IN HUMAN T-CELL LYMPHOTROPIC VIRUS TYPE I-ASSOCIATED MYELOPATHY, Archives of neurology, 52(3), 1995, pp. 276-280
Citations number
36
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
00039942
Volume
52
Issue
3
Year of publication
1995
Pages
276 - 280
Database
ISI
SICI code
0003-9942(1995)52:3<276:EMEOIC>2.0.ZU;2-I
Abstract
Objective: To investigate the expression of inflammatory cytokine mess enger RNA (mRNA) in peripheral blood mononuclear cells of patients wit h human T-cell lymphotropic virus type I (HTLV-I)-associated myelopath y (HAM). Patients: Seventeen patients with HAM, 18 HTLV-I-seropositive carriers, and 10 seronegative individuals were studied. Main Outcome Measure: We compared the expression of tumor necrosis factor alpha (TN F-alpha), granulocyte-macrophage colony-stimulating factor (GM-CSF), i nterferon 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 transcript ase-polymerase chain reaction products of TNF-alpha, GMCSF, 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 cytokine s was detected in all. patients with HAM compared with only 21.4% of H TLV-I-seropositive carriers. By contrast, there was no significant dif ference in mRNA expression of IFN-alpha, IFN-beta, and IL-1 beta among patients with HAM, HTLV-I-seropositive carriers, and HTLV-I-seronegat ive controls. Conclusions: An exaggerated mRNA expression of several i nflammatory cytokines, including TNF-alpha, GM-CSF, IFN-gamma, and IL- 1 alpha, was demonstrated in peripheral blood mononuclear cells of pat ients with HAM. Moreover, transcripts of these cytokines were simultan eously up-regulated in patients with HAM, suggesting that an inflammat ory state in the central nervous system may be related to the pathogen esis of HAM.