The pathogenicity of Bacillus anthracis, the bacterium that causes anthrax, is associated with the two toxins it secretes. The overall goal of this project is advance the understanding the role ET plays in anthrax pathogenesis. The proposed research herein aims to identify role ET plays in receptor expression as well as the effect ET has on dendritic cells. In order to determine the role ET plays in receptor levels, receptor levels will be monitored in vivo and in vivo following toxin challenge. As part of this work availability of receptor in vivo will be determined, providing further insight as to what tissues toxin has access. In addition, this work aims at addressing the effect ET has on dendritic cells as a means of understanding the impact ET has on these cells ability in mounting an immune defense. Mounting evidence suggests that both toxins target immune cells in an effort to dismantle host defenses to permit outgrowth of bacilli. The work proposed here will further advance the efforts in understanding how much of a blow the immune system is dealt upon infection, and specifically how ET contributes. ? ? ?
| Larabee, Jason L; Maldonado-Arocho, Francisco J; Pacheco, Sergio et al. (2011) Glycogen synthase kinase 3 activation is important for anthrax edema toxin-induced dendritic cell maturation and anthrax toxin receptor 2 expression in macrophages. Infect Immun 79:3302-8 |
| Eshraghi, Aria; Maldonado-Arocho, Francisco J; Gargi, Amandeep et al. (2010) Cytolethal distending toxin family members are differentially affected by alterations in host glycans and membrane cholesterol. J Biol Chem 285:18199-207 |
| Maldonado-Arocho, Francisco J; Bradley, Kenneth A (2009) Anthrax edema toxin induces maturation of dendritic cells and enhances chemotaxis towards macrophage inflammatory protein 3beta. Infect Immun 77:2036-42 |
