A parasite with the guts of a burglar.

A parasite with the guts of a burglar

A lot of unfriendly parasites would likenothing better than to take up residence inside some of the body's calls, where they can ensure their existence by feeding happily on their host. There are even some cells in the body that encourage such visitors. The cells, called macrophages, act like janitors, sweeping up bacteria and dead tissue. But these cells are probably the last place an unfriendly invader wants to be--once attached to the cell, the parasites are usually doomed, as a macrophage respiratory burst generates toxic oxygen molecules to destroy the attacker.

But two scientists now believe theymay have uncovered the way in which one parasite not only gets into a macrophage, but also avoids death once inside. David M. Mosser and Paul J. Edelson of Cornell University Medical College in New York City have found that Leishmania major, which causes parasitic diseases common to the tropics, uses one of the body's nine components of complement --proteins that help destroy foreign invaders--to stay alive. Leishmania, which first live in an insect before changing form and transferring to a warm-blooded host, often affect children and are responsible for mild to fatal lesions and ulcers on the body. The diseases caused by leishmania have been cited by the World Health Organization and others as one of the five major health parasitic scourges worldwide.

Since macrophages try to make mincemeatout of microorganisms upon binding, the trick for a parasite is to get past the cell's defense mechanism and into its new home. "Leishmania have to have a way of ringing the doorbell without triggering the burglar alarm,' Edelson says. Although it has been known that leishmania and other organisms, such as Toxoplasma gondii, have learned how to enter a macrophage without triggering a burst, Edelson believes this is the first time scientists have shown how leishmania achieve that feat. "Leishmania have figured out,' Edelson says, that a specific receptor on a specific complement can be "the doorbell.'

Edelson speculates leishmania are successfulperhaps because not all receptors trigger the respiratory burst, and leishmania have figured out which one bypasses the deadly process. Edelson believes the third component of complement (C3) is reponsible for getting leishmania into the cell and decreasing the effects of respiratory burst once there. By binding to a specific receptor, leishmania are able to trigger the unlocking of the door. Complement normally works, in part, by coating an invader for ingestion by a macrophage. In this case, the parasites have learned to change complement from adversary to ally. And if successful in disarming the cell, leishmania multiply to the point where they burst their host.

The study, published in the May 28NATURE, looked at the number of surviving intracellular organisms at 24 and 48 hours following ingestion of leishmania into about a million mouse macrophages. In the absence of the serum complement, more than 95 percent of the parasites were killed once ingested by the macrophages. Those exposed to serum complement, however, increased their chances of survival 10-fold.

Mosser and Edelson believe it could becommon practice for leishmania and perhaps other intracellular parasites to activate C3 and gain entrance into cells.

The findings might be used to helpresearchers discover ways to prevent invading organisms from picking up the complement they need to penetrate the cell or to help program cells to initiate a respiratory burst against any invader.