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Scientists Find Potential Weapon Against Tuberculosis Infection

Posted by tumicrobiology on December 14, 2006

The discovery of a unique copper-repressing protein in the bacterium that causes tuberculosis in humans may pave the way toward new strategies for halting tuberculosis infection.

Scientists have known that when macrophages – the host’s immune cells – swallow an invading bacterium, they dump excessive amounts of copper onto the invader in an effort to kill it. While all cells need copper to function, too much of the metal ion causes cell death.

“But the invaders fight back with their own defense,” says Adel Talaat, a microbiologist at the University of Wisconsin-Madison School of Veterinary Medicine. “They block the excess copper.”

In a paper published in the January 2007 issue of Nature Chemical Biology, Talaat and colleagues from Texas A&M University and University of Saskatchewan in Saskatoon, Canada describe a unique protein repressor that they have identified as the mechanism used by invading bacterium cells to fight off the host’s copper attack.

Prior to the discovery of this repressor protein, scientists did not know exactly how invading bacterium protected themselves from copper ions used by the body as a defense against infection.

“With this discovery, we can now pursue ways to deactivate the repressor protein,” says Talaat. “Our goal is to disable the tuberculosis bacterium from fighting back against the host body’s defense mechanisms, so that we can stop tuberculosis.”
Source: University Of Wisconsin-Madison


3 Responses to “Scientists Find Potential Weapon Against Tuberculosis Infection”

  1. Fungal infection host protein found

    South African and Japanese scientists have, independently, demonstrated the importance of a host protein in recognizing the presence of fungal infections.

    Pathogenic fungi can cause life-threatening infections in individuals with immunodeficiencies, such as those with advanced HIV disease.

    The two independent groups led by Gordon Brown of the University of Cape Town in South Africa and Yoichiro Iwakura at the University of Tokyo produced mice lacking the protein Dectin-1 — a cell-surface protein implicated in immune responses to fungal infections.

    Both studies show mice lacking Dectin-1 are relatively normal except when infected with fungi, which causes more lethality in the mutant mice. The authors also evaluated the types of blunted immune responses that occur in the mutant mice and show only specific immune functions are defective.

    Both studies are presented in the January issue of the journal Nature Immunology.

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