PMID- 7872881
OWN - NLM
STAT- MEDLINE
DCOM- 19950324
LR  - 20190717
IS  - 0003-9942 (Print)
IS  - 0003-9942 (Linking)
VI  - 52
IP  - 3
DP  - 1995 Mar
TI  - Exaggerated messenger RNA expression of inflammatory cytokines in human T-cell 
      lymphotropic virus type I-associated myelopathy.
PG  - 276-80
AB  - 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.
FAU - Watanabe, H
AU  - Watanabe H
AD  - First Department of Internal Medicine, Nagasaki, Japan.
FAU - Nakamura, T
AU  - Nakamura T
FAU - Nagasato, K
AU  - Nagasato K
FAU - Shirabe, S
AU  - Shirabe S
FAU - Ohishi, K
AU  - Ohishi K
FAU - Ichinose, K
AU  - Ichinose K
FAU - Nishiura, Y
AU  - Nishiura Y
FAU - Chiyoda, S
AU  - Chiyoda S
FAU - Tsujihata, M
AU  - Tsujihata M
FAU - Nagataki, S
AU  - Nagataki S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Arch Neurol
JT  - Archives of neurology
JID - 0372436
RN  - 0 (Cytokines)
RN  - 0 (Interferon-alpha)
RN  - 0 (Interleukin-1)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 77238-31-4 (Interferon-beta)
RN  - 82115-62-6 (Interferon-gamma)
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Base Sequence
MH  - Cytokines/*genetics
MH  - Female
MH  - Granulocyte-Macrophage Colony-Stimulating Factor/genetics
MH  - Humans
MH  - Interferon-alpha/genetics
MH  - Interferon-beta/genetics
MH  - Interferon-gamma/genetics
MH  - Interleukin-1/genetics
MH  - Male
MH  - Middle Aged
MH  - Molecular Sequence Data
MH  - Paraparesis, Tropical Spastic/*genetics
MH  - RNA, Messenger/*metabolism
MH  - Tumor Necrosis Factor-alpha/genetics
EDAT- 1995/03/01 00:00
MHDA- 1995/03/01 00:01
CRDT- 1995/03/01 00:00
PHST- 1995/03/01 00:00 [pubmed]
PHST- 1995/03/01 00:01 [medline]
PHST- 1995/03/01 00:00 [entrez]
AID - 10.1001/archneur.1995.00540270068021 [doi]
PST - ppublish
SO  - Arch Neurol. 1995 Mar;52(3):276-80. doi: 10.1001/archneur.1995.00540270068021.