This study investigates the role of Th17 cells in demyelination and paralysis in a mouse model. By injecting Th17 cells and a bacterial toxin, the research explores the inflammatory response and its effects on nerve signal transmission.
Begin with a syringe containing T-helper or Th17 cells capable of recognizing an aquaporin-4 protein of astrocytes in the CNS, including the spinal cord, which plays a role in signal transmission to the brain.
Inject these Th17 cells into the tail vein of a restrained mouse. The cells enter the bloodstream and circulate throughout the body.
Simultaneously, intraperitoneally administer a bacterial toxin derived from the Bordetella pertussis.
The toxin disturbs the endothelial barrier of blood vessels and allows Th17 cells to infiltrate the spinal cord.
The infiltrated Th17 cells interact with the astrocytes expressing the aquaporin-4 and become activated.
These activated cells release pro-inflammatory cytokines, which causes the infiltration of mononuclear immune cells, including macrophages.
Macrophages release inflammatory molecules that damage the myelin sheath of the surrounding nerve fibers.
This demyelination disrupts nerve signal transmission, leading to tail stiffness and restricted hind limb movement, indicating the onset of paralysis.
Within one hour of their collection, transfer the cells into a 1-milliliter syringe and deliver 200 microliters of cells to each recipient animal intravenously through the tail vein. Then, inject each mouse intraperitoneally immediately, and two days later, with 200 nanograms of B. pertussis toxin diluted in 200 microliters of PBS.
繁體中文
