Other Publications (1)
Articles by Jillian C. Nissen in JoVE
Culturing Microglia from the Neonatal and Adult Central Nervous System Robert Bronstein*1,2, Luisa Torres*2,3, Jillian C. Nissen*2,3, Stella E. Tsirka2 1Program in Neuroscience, Stony Brook University, 2Department of Pharmacological Sciences, Stony Brook University, 3Program in Molecular and Cellular Pharmacology, Stony Brook University We outline methods for the efficient and quick isolation/culture of viable microglia from the neonatal cerebral cortex and adult spinal cord. The dissection and plating of cortical microglia can be accomplished within 90 minutes, with the subsequent microglial harvest taking place ~ 10 days following the initial dissection.
Other articles by Jillian C. Nissen on PubMed
Tuftsin Promotes an Anti-inflammatory Switch and Attenuates Symptoms in Experimental Autoimmune Encephalomyelitis PloS One. 2012 | Pubmed ID: 22529957 Multiple sclerosis (MS) is a demyelinating autoimmune disease mediated by infiltration of T cells into the central nervous system after compromise of the blood-brain barrier. We have previously shown that administration of tuftsin, a macrophage/microglial activator, dramatically improves the clinical course of experimental autoimmune encephalomyelitis (EAE), a well-established animal model for MS. Tuftsin administration correlates with upregulation of the immunosuppressive Helper-2 T cell (Th2) cytokine transcription factor GATA-3. We now show that tuftsin-mediated microglial activation results in shifting microglia to an anti-inflammatory phenotype. Moreover, the T cell phenotype is shifted towards immunoprotection after exposure to tuftsin-treated activated microglia; specifically, downregulation of pro-inflammatory Th1 responses is triggered in conjunction with upregulation of Th2-specific responses and expansion of immunosuppressive regulatory T cells (Tregs). Finally, tuftsin-shifted T cells, delivered into animals via adoptive transfer, reverse the pathology observed in mice with established EAE. Taken together, our findings demonstrate that tuftsin decreases the proinflammatory environment of EAE and may represent a therapeutic opportunity for treatment of MS.