PMID- 2681538 OWN - NLM STAT- MEDLINE DCOM- 19891201 LR - 20190724 IS - 0022-510X (Print) IS - 0022-510X (Linking) VI - 92 IP - 2-3 DP - 1989 Sep TI - Neurotoxic activity in HTLV-I carrier lymphocyte culture. PG - 169-80 AB - A close association between human T-lymphotropic virus type I (HTLV-I) infection and a group of chronic myelopathies of unknown etiology has recently been established and the name "HTLV-I associated myelopathy" (HAM) has been coined. Although the mechanism of neural tissue damage in HAM remains virtually unknown, several lines of evidence suggest the involvement of a soluble factor(s) including cytokines and viral proteins in the disease process. In this study, we examined cytopathic effects of the supernatants from 6 HTLV-I carrier human T lymphocyte cell lines on 4 human and one murine neuroblastoma cell lines, and 2 human glioma cell lines. Among 6 lymphocyte cell culture supernatants, only 1 from MT-2 cell culture repeatedly exerted cytopathic effects on human neuroblastoma cells, particularly on IMR-32 cells: marked retraction of neurites leading to cellular clumping. This activity was neither abolished by treatment of the medium at 80 degrees C for 30 min or by UV-irradiation, nor was it neutralized by anti-HTLV-I antibodies. The MT-2 supernatant also induced mild cytopathic changes in 2 other human neuroblastoma cell lines and 2 human glioma cell lines. This activity was abolished by treatment of the medium at 80 degrees C for 30 min but not at 56 degrees C for 30 min. Myelinated murine cerebellum explants and other cell lines showed no morphological changes when incubated with the MT-2 supernatant. In addition, the growth of THP-1 cells, a monocyte/macrophage lineage cell line, was remarkably suppressed when maintained in the MT-2 conditioned medium, accompanied by enhancement of phagocytic activity. The THP-1 conditioned medium, on the other hand, suppressed tumor necrosis factor (TNF) activity detected in the MT-2 culture. These observations suggest that HTLV-I induced cytokines may directly act on neural cells, but their action appears to be regulated by the intricate interactions of lymphocytic and monocytic cells. FAU - Terunuma, H AU - Terunuma H AD - Department of Neurological Sciences, Tohoku University School of Medicine, Sendai, Japan. FAU - Iwasaki, Y AU - Iwasaki Y FAU - Tsukamoto, T AU - Tsukamoto T FAU - Konno, H AU - Konno H FAU - Yamamoto, T AU - Yamamoto T FAU - Ohara, Y AU - Ohara Y LA - eng PT - Journal Article PL - Netherlands TA - J Neurol Sci JT - Journal of the neurological sciences JID - 0375403 RN - 0 (Biological Factors) RN - 0 (Cytokines) RN - 0 (Neurotoxins) RN - 0 (Tumor Necrosis Factor-alpha) RN - 0 (Viral Proteins) SB - IM MH - Animals MH - Biological Factors/*metabolism/pharmacology MH - Cell Line MH - Cell Survival/drug effects MH - Cytokines MH - HTLV-I Infections/*metabolism MH - Humans MH - Mice MH - Neurotoxins/*metabolism/pharmacology MH - Tumor Cells, Cultured/*drug effects MH - Tumor Necrosis Factor-alpha/pharmacology MH - Viral Proteins/*metabolism/pharmacology EDAT- 1989/09/01 00:00 MHDA- 1989/09/01 00:01 CRDT- 1989/09/01 00:00 PHST- 1989/09/01 00:00 [pubmed] PHST- 1989/09/01 00:01 [medline] PHST- 1989/09/01 00:00 [entrez] AID - 0022-510X(89)90134-2 [pii] AID - 10.1016/0022-510x(89)90134-2 [doi] PST - ppublish SO - J Neurol Sci. 1989 Sep;92(2-3):169-80. doi: 10.1016/0022-510x(89)90134-2.