When they gave the PLSJL mice the anti-inflammatory steroid hormone DHEA, the brain inflammation decreased, the barriers permeability lessened, and the death rate more than doubled.
The researchers thought that if some rabies-infected PLSJL mice died because the virus overwhelms the immune system T and B cells already in the brain and CNS, then opening the barrier even more would enable more immune cells to reach CNS tissue and fight the virus. They subsequently gave animals experimental autoimmune encephalitis (EAE), which causes an inflammatory response and the barrier to open. As a result, a higher percentage of animals survived the infection.
Halting rabies in the brain
In the future, one of the things we want to do is tone down the inflammatory response caused by EAE and minimize the pathogenesis, yet deliver immune cells to the CNS, says Dr. Hooper, who is also associate director of Jeffersons Center for Neurovirology. The trick to survival might be to open the barrier and deliver effectors to the CNS.
The data suggest that the CNS cells are developing T and B cells effectively, but that delivery to the CNS is impaired, Dr. Hooper explains. It might mean that the communication between the CNS and the immune system is somehow blocked. Perhaps when the disease gets further along, it triggers certain hormones that prevent the brain barrier from opening in response to immune signals. Were trying to develop a better way to open the barrier and let these immune cells in.
While they would like t
|Contact: Steve Benowitz|
Thomas Jefferson University