Interactions between rat brain astrocytes and human mononuclear cells to produce MCP-1 ( monocyte chemoattractant protein-1 ) ; interleukin-2 and interleukin-2 receptor

• Main Authors: Su, Jen-Jen, 蘇真真
• Other Authors: Yu, Chia-Li
• Format: Others
• Language: zh-TW
• Published: 2002
• Online Access: http://ndltd.ncl.edu.tw/handle/79034443306981886415

碩士 === 國立臺灣大學 === 分子醫學研究所 === 90 === Monocyte chemoattractant protein —1 ( MCP-1 ) is belonged to chemokine βfamily. Astrocytes are part of glial system of the central nervous system( CNS ). The foot process of astrocyte is responsible for molecular transport and composes part of blood-brain-barrier ( BBB ). Chemokines are thought to be related with tissue inflammation, infection and tumor. As about the CNS infection, chemokines are thought to attract leukocytes to tissue then induce inflammation. In some animal model; MCP-1 is identified to induce CNS inflammation. Interleukin-2 ( IL-2 ), produced by T lymphocyte, is a kind of T-/B- lymphocyte growth factor. Except being the important role in inflammation, IL-2 also shows significant correlation with multiple sclerosis ( MS ) in a series of studies. Anyway, what kind of signals to activate astrocyte or produce MCP-1 is still unknown. In our study, we used cell culture and MTT test to test the survival of rat neroblastoma cell ( RBA-1 ); ELISA to quantity the production of MCP-1 and IL-2 from super ant; RT-PCR to estimate UPAR expression and flow cytometry to estimate chemokine receptor. We wish to clarify the interaction between monocyte and RBA-1 and the effect to produce IL-2 and MCP-1. Then we estimate MCP-1 form co-culture of RBA-1 with CSF from lot patients with neurological diseases for the possible pathogenesis. In our experiment; we found there is significant increase of MCP-1 after RBA-1 co-culture with MNC. Also it is same when we used transwell to separate both kinds of cells. And we found TNF-α,IFN-βand IL-6 influence RBA-1 to produce more MCP-1. We also had more IL-2 and sIL-2R produced when co-culture with RBA-1 and MNC. As to UPAR experiment, we found no UPARmRNA expression when RBA-1 alone. According to the above experiments, we conclude that MCN can make RBA-1 produce increased MCP-1 even without direct contact; then MCP-1 activate MNC to produce IL-2, and it will make an amplification recruitment to make further inflammation.