(Ivanhoe Newswire) – After spinal cord injury, certain immune cells collect in the spinal fluid and release high levels of antibodies. A new study by neuroscientists at The Ohio State University Medical Center may have solved the mystery of what these antibodies do there. Researchers found that the antibodies may actually worsen and extend the spinal cord damage.
The antibodies first attach to nerve cells and other elements of the nervous system. Then, other components of the immune system attack the cells and substances marked by the antibodies as if they were infectious agents or foreign material.
"Our findings suggest that inhibiting or depleting B lymphocytes, the cells that produce antibodies, may promote healing and reduce the long-term effects of spinal cord injury," study leader Phillip G. Popovich, professor of neuroscience and of molecular virology, immunology and medical genetics and director of the Center for Brain and Spinal Cord Repair, was quoted as saying. "They may also help explain why the central nervous system does not repair itself efficiently and why other impairments often follow spinal cord injury."
For this study, Popovich, first author Daniel P. Ankeny, and research associate Zhen Guan, used mice that were anesthetized and given a moderately severe spinal injury that mimics a contusion-type spinal injury in humans.
One group of injured mice had a normal immune system, with
antibody-producing B cells. A second group of mice was identical to
the first, except that they lacked B cells, and therefore produced
no antibodies.
Nine weeks after spinal cord injury, the researchers compared
the two groups. They found that, on average, the area of spinal
cord damage in mice without antibodies was 30 percent smaller than
the damaged area in mice with antibodies.
The researchers found that B cells and antibodies had
accumulated around the spinal cord in the normal mice but not in
the other group, and that antibodies had attached to damaged areas
of the spinal cord.
They also found substantially higher levels of antibodies in
the bloodstream of the normal group after spinal cord injury than
were present before injury.
To learn whether these antibodies could, on their own, damage
the spinal cord, the investigators purified them from the blood of
injured mice and microinjected them into one side of the spinal
cord of uninjured normal mice. Within 48 hours, the hind leg on the
side of the injection site became paralyzed, and remained partially
so after one week. The animals also showed loss of neurons and
other damage to the spinal cord.
The investigators speculate that because the antibodies are
produced systemically, they also may damage other tissues. Popovich
noted that, along with paralysis, individuals with spinal cord
injury may also have systemic problems, such as chronic bladder
problems. These are usually attributed to chronic catheterization
and loss of bladder control, he says. "But that doesn't explain
changes that also occur in the kidneys. It may be that antibodies
are targeting antigens within the kidney and causing kidney
damage."
