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Published on: September 26, 2012
Exaggerated messenger RNA expression of inflammatory cytokines in human T-cell lymphotropic virus type I-associated
H Watanabe1, T Nakamura, K Nagasato
1First Department of Internal Medicine, Nagasaki, Japan.
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 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.
Insights
Patients with human T-cell lymphotropic virus type I-associated myelopathy (HAM) show increased inflammatory cytokine mRNA. This suggests a link between elevated cytokine expression and the development of HAM.
Area of Science:
- Immunology
- Neuroscience
- Virology
Background:
- Human T-cell lymphotropic virus type I (HTLV-I) infection is linked to neurological diseases.
- HTLV-I-associated myelopathy (HAM) is a chronic inflammatory condition affecting the spinal cord.
Purpose of the Study:
- To investigate the expression of inflammatory cytokine messenger RNA (mRNA) in peripheral blood mononuclear cells (PBMCs) of patients with HAM.
- To compare cytokine mRNA levels between HAM patients, HTLV-I carriers, and healthy controls.
Main Methods:
- Studied 17 HAM patients, 18 HTLV-I carriers, and 10 seronegative controls.
- Analyzed mRNA expression of TNF-alpha, GM-CSF, IFN-gamma, IL-1 alpha, IL-1 beta, IFN-alpha, and IFN-beta using reverse transcriptase-polymerase chain reaction (RT-PCR).
Main Results:
- Significantly higher incidences of TNF-alpha, GM-CSF, IFN-gamma, and IL-1 alpha mRNA in HAM patients compared to controls.
- All HAM patients exhibited simultaneous mRNA expression of three or more of these four cytokines.
- No significant differences in IFN-alpha, IFN-beta, and IL-1 beta mRNA expression were observed across groups.
Conclusions:
- Exaggerated mRNA expression of specific inflammatory cytokines (TNF-alpha, GM-CSF, IFN-gamma, IL-1 alpha) in PBMCs of HAM patients.
- Simultaneous up-regulation of these cytokine transcripts in HAM patients suggests a role in disease pathogenesis.
- The findings indicate a potential inflammatory state in the central nervous system contributing to HAM development.
