The virulence of Anthrax depends on two factors: the bacterial capsule and the toxin complex. All virulent strains of B. anthracis form a single antigenic type of capsule consisting of a poly-D-glutamate polypeptide. The unusual poly-D-glutamyl acid capsule is itself nontoxic, but functions to protect the organism against the bactericidal components of serum and phagocytes and against phagocytic engulfment. Capsule production depends on a 60-

It is known that the germination of spores within the host is the initial step of Anthrax infection. The alveolar macrophage has been observed as the primary site of B. anthracis germination in a murine inhalation infection model. Macrophage cells sample the environment within us, identify bacteria and viruses, and produce signals that can activate the immune system. Sometimes these signals are produced in abnormally high amounts, and can damage to our system. Tumor necrosis factor is one such substance, and Anthrax lethal toxin can cause macrophages to release this in dangerous amounts. Dehydroepiandrosterone (DHEA) and melatonin, given either separately or together, moderated this toxic effect of Anthrax lethal toxin. Also, soy has been found to possess a beneficial property when dealing with the pathogenicity of Anthrax. Soy, as any plant, contains many substances that affect our physiology. Genistein is one such substance. It has beneficial effects on menopausal symptoms and blood clotting. It reduces the risk of cancer and reduces toxins in the intestine. This study in Korea showed that genistein reduced the toxicity of Anthrax lethal toxin.

megadalton plasmid, pX02; its transfer to nonencapsulated B. anthracis via transduction produces the encapsulated phenotype. The capsule plays its most important role during the establishment of the infection and a less significant role in the terminal phases of the disease, which are mediated by the Anthrax toxin.

These results imply that the cytolytic effect of the toxin is mediated by ROIs. Additionally, cytokine production and consequent pathologies showed partial dependence on macrophage ROIs. Antioxidants moderately inhibited toxin-induced cytokine production in vitro, and mice pretreated with N-acetyl-L-cysteine or mepacrine showed partial protection against lethal toxin. Thus, it is assumed that ROIs are involved in both the cyto

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