Such therapies might have the potential to protect against anthrax during the late stages of the disease, after antibiotics have lost their therapeutic value, they added.
The team found that human cells deficient in the so-called LDL receptor-related protein (LRP6) become resistant to anthrax toxin. Furthermore, antibodies against LRP6 protected cells from anthrax toxicity, reported study authors Wensheng Wei and Stanley Cohen of the Stanford University School of Medicine in collaboration with others at Stanford and the National Institutes of Health. The level of anthrax protection afforded by the antibodies rose with increasing dose.
Anthrax is a lethal disease of humans and other animals caused by the spore-forming bacteria Bacillus anthracis, which has been the focus of biological interest and bioterrorism concern. The virulence of the bacteria depends on separate complexes formed by interaction of a carrier protein, protective antigen, with lethal and edema factors responsible for the toxic effects and swelling that impairs the host's immune response.
In the current study, the researchers inactivated genes randomly in human cells. They then examined the mutated cells for resistance to anthrax toxin in an effort to identify host genes that have important roles in infection, with the hope of finding possible new targets for therapies aimed at the host instead of the bacteria. The method allows for the identification of required host cell genes without pre-conceptions about their potential to play a role, the study authors said.
The study revealed that LRP6 acts as a co-receptor, enabling cells to take up anthrax toxin through its interactions with two distinct cell- surface proteins earlier shown to bi