PLGA-Cy5 labelled polymer from PolySciTech used in development of anti-inflammatory treatment of spinal cord injury

 

One of the problems post spinal-cord injury is that inflammation (swelling, etc.) complicates and prevents the healing process. Targetted delivery of MAPK-activated protein kinase-2 (MK2) inhibitor can reduce the damaging effects of this inflammation. Recently researchers at Houston Methodist Academic Institute utilized PLGA-CY5 fluorescent (Cat# AV034) polymer from PolySciTech division of Akina (www.polyscitech.com) to create fluorescent nanoparticles for tracking purposes. This research holds promise to improve therapeutic outcomes for cpinal cord injury and reduce the incidence of associated paralysis. Read more: Stigliano, Cinzia, Allison Frazier, and Philip J. Horner. "Modulation of Neuroinflammation Via Selective Nanoparticle‐Mediated Drug Delivery to Activated Microglia/Macrophages in Spinal Cord Injury." Advanced Therapeutics: 2200083. https://onlinelibrary.wiley.com/doi/abs/10.1002/adtp.202200083

“Abstract: Inflammation after spinal cord injury (SCI) is characterized by immune cell invasion and activation, combined with inflammatory mediator release that worsens outcomes following primary trauma. Effective therapies targeting neuroinflammation remain an unmet need, and modulation of the injury microenvironment to induce a comprehensive pro-regenerative response is an attractive therapeutic approach. Given its crucial role in cell stress and inflammation after SCI, we focused on the potential of pharmacologically targeting MAPK-activated protein kinase-2 (MK2) to modulate the response of microglia/macrophages after injury. We developed nanoparticles (NPs) containing an MK2 inhibitor for specific targeting of microglia/macrophages. NPs selectively targeted and modulated activated microglia/macrophages in vitro and in a rat model of SCI. NPs in the acute injury setting reduced the pro-inflammatory cytokine IL-6 and increased the anti-inflammatory cytokine IL-10. Importantly, NPs had a significant effect on microglia/macrophage distribution and accumulation, leading to an ∼65% reduction of immune cells around the injury. Lastly, microglia/macrophage populations with activated morphology were significantly reduced compared to resting or ramified cells around the lesion site. Our strategy exhibits potential therapeutic efficiency and specificity for local, pharmacologic manipulation of activated microglia/macrophages, and is a versatile tool to manage acute inflammation and glia plasticity after central nervous system trauma.”