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March 1995

Exaggerated Messenger RNA Expression of Inflammatory Cytokines in Human T-Cell Lymphotropic Virus Type I—Associated Myelopathy

Author Affiliations

From the First Department of Internal Medicine, Nagasaki (Japan) University School of Medicine (Drs Watanabe, Nakamura, Nagasato, Shirabe, Ohishi, Ichinose, Nishiura, and Nagataki); the Nagasaki Atomic Bomb Hospital, Japan Red Cross (Dr Chiyoda); and School of Allied Medical Sciences, Nagasaki University (Dr Tsujihata).

Arch Neurol. 1995;52(3):276-280. doi:10.1001/archneur.1995.00540270068021

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).

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 α (TNF-α), granulocytemacrophage colony-stimulating factor (GM-CSF), interferon alpha (IFN-α), IFN-β, and IFN-γ, and interleukin 1α (IL-1α) and IL-1β by reverse transcriptase—polymerase chain reaction.

Results:  In patients with HAM, the reverse transcriptase—polymerase chain reaction products of TNF-α, GM-CSF, IFN-γ, and IL-1α 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-α, IFN-β, and IL-1 β among patients with HAM, HTLV-I—seropositive carriers, and HTLV-I—seronegative controls.

Conclusions:  An exaggerated mRNA expression of several inflammatory cytokines, including TNF-α, GM-CSF, IFN-γ, and IL-1α, 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.

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