Anti-bodies are proteins that are produced by the immune system to safeguard the human body against bacteria and viruses. Stanford is the first institute to show that antibodies are not only warriors fighting infectious diseases but as well nurses. This has been shown by researchers at Stanford University School of Medicine.
The lack of antibodies in our central nervous system (spinal cord and brain) can be a key factor explaining why nerve damage is not naturally repaired. This piece of information could help to develop treatment for spinal-cord trauma as well as stroke.
The study performed on mice was published online 14th of June 2010 in the Proceedings of National Academy of Science. Stanford’s scientists were able to show the significance of antibodies in alleviating nerve damage in our peripheral nervous system (nerve tissues outside our spinal cord & brain, like sciatic nerve). This is the first study to demonstrate the nursing role of antibodies.
The study does as well prove that most (not all) antibodies can repair nerve damage. This implies that developing these proteins could significantly help to induce treatment to repair damage caused by spinal cord or stroke injuries.
Ben Barres, MD PhD, professor, chair of neurobiology and senior study author says that it is unknown why the central nervous system is unable regenerate after damage while injuries in the peripheral nervous system do easily regenerate. This stirred the interest of his team to understand why the two nervous systems were different. It was found that antibodies, categorised as large proteins have difficulties in reaching the spinal cord and brain (there exists a blood-brain barrier and blood-spinal cord barrier for the brain and spinal cord, respectively). Yet, antibodies can easily access our peripheral nervous system.
The function of nerve cells is commonly defined as sending electrochemical impulses to various far-reaching distances through tubular projections known as axons. These axons have an insulating layer, of a type of fatty compound known as myelin.
Barres said that “After nerve injury, the degenerating myelin downstream from the injury is rapidly cleared in the peripheral, but not the central nervous system,” Any damage to the spinal cord or human brain will cause the production of degenerating myelin, which will simply remain at its location for the rest of the lifetime of the person. In any other region such as for sciatic nerve the degenerating myelin disappears after a week if not even less.
Former Student in Barres’ lab, Mauricio Vargas, MD, PhD and Junryo Watanabe, PhD, a postdoctoral researcher in the lab had been thinking of the association between degenerative myelin and antibodies. So they used some mutated mice which lacked the ability to produce antibodies. It was shown that injuries to the sciatic nerve were not repaired. However, once these injured mutant mice were injected with antibodies, the myelin was removed and the sciatic nerve was repaired.
Vargas, who is actually on an internship at White Memorial Medical Center in Lost Angeles, says that antibodies have been known to contribute significantly to the disposal of aging red blood cells. However, it is first time that antibodies have been shown to be involved in repairing injuries.
Vargas did also give further insight to show how this really occurred. “We showed that antibodies grab onto degenerating myelin downstream from the site of the nerve injury, coating the myelin and tagging it for clearance by voracious immune cells called macrophages,”
“Big eater” is the Greek translation of macrophage. These fatty substances do work to conceal antibody-tagged to bacteria and diseased cells.
Several standard laboratory tools were used like unique staining techniques. The observation showed that macrophages eliminate antibody-tagged degenerating myelin in nerve-injured regions. The removal of myelin was significantly improved when the mice lacking antibodies was injected with antibodies from healthy mice.
It did not matter whether the antibodies were taken from mice that had previously suffered from injuries or not. This means that antibodies are naturally able to remove the degenerating myelin, and these antibodies are thus not called-upon only after injury.
The injection of these readily available natural antibodies accelerated the repairing mechanism of the mice. It would take the body a few weeks to produce antibodies able to fight these bacterial infections.
In a further test, Barres and his team injected a dose of antibody into injured mice but this time the protein was aimed only at the myelin. The result was that the nerves injured got repaired. However, injecting antibodies not related to myelin did not have any effect. This proves that only certain types of antibodies will be able to improve the state of degenerating myelin. The most effective once are those that are found in the peripheral nervous system.
Fortunately, antibodies able to eradicate myelin are distinguishable. The antibodies associated with degenerating myelin had a radically different surface structure compared to other antibodies in our immune system.
According to Barres, these findings might provide promising hopes for repairing damaged in our central nervous system. This would include damages caused by spinal cord injury or stroke. A potential way to use the antibodies would be to bypass blood-brain barriers and then introduce the anti-degenerating-myelin proteins immediately to the spinal fluid.
Zhigang, PhD, associate professor of neurology at Harvard Medical School says this study contributed significantly in understanding why some nerve tissues regenerate and other not. In other words, the study shows why peripheral nervous system repairs itself while our central nervous system is unable to.
Now the mechanism is understood. The only thing left is to find a strategy to accelerate the clearance of myelin in our brain. This could induce the regeneration of injuries to both peripheral and central nervous system.
Wed, Aug 4, 2010
Nanotechnology, Stem cells