In Anura Rambukkana's study, published in Nature Medicine, showed that the leprosy bacteria, Mycobacterium leprae, attaches to myelinated Schwann cells and induces rapid demyelination. This demyelination can occur in the absence of immune cells, which is the cause of demyelination in neurodegenerative diseases, but the process is chronic and relatively slow despite high levels of the M. Leprae.
Type-1 leprosy reactions are idiopathic episodes of strongly increased inflammation and cell-mediated immune reactivity which are frequently accompanied by acute inflammation of peripheral nerves. This peripheral inflammation often leads to extensive and irreversible nerve damage. Immunosuppressive drugs are often a treatment to prevent further nerve damage.
This information suggests that inflammatory immune reactions play an important role in leprosy nerve damage and that the mere presence of M. leprae does not explain the full extent of leprosy nerve damage. Inflammatory responses seem to be necessary for the complete manifestation of demyelination, like in other neurodegenerative diseases.
Though the mechanismas are not entirely clear, it is believed that there are two phases of M. leprae actions. The early phase consists of specific targeting of peripheral nerves and contact dependent demyelination. The other phase consists of increase immunity and inflammation, where acute and extensive nerve damage happens, mostly contributed by cytokines and immune effector cells.
The human immune response plays an important role in the full expression of leprosy nerve damage.
http://www.sciencemag.org/cgi/content/full/296/5569/927?ck=nck
Subscribe to:
Post Comments (Atom)
2 comments:
Thanks for the nice summary on leprosy! I read the link to the article and was interested by the fact that the bacteria caused significant demyelination in Schwann cell cultures just 24 hours after infection. This seems to support the hypothesis of a 2-phase mechanism. It was also interesting to read that irradiated (dead) bacteria still caused demyelination, both in vitro and in vivo. This seemed to suggest that a component of the bacterial cell wall was responsible for nerve damage. This is an important finding for leprosy patients who have been cured of the bacteria, yet still experience nerve damage. Thanks again for the post!
Post a Comment