作者: Elizabeth A. Henderson , Leandra O. Gonzalez , Stella Hartmann , Christopher P. Klimko , Jennifer L. Shoe
DOI: 10.1371/JOURNAL.PPAT.1008836
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摘要: Anthrax is a major zoonotic disease of wildlife, and in places like West Africa, it can be caused by Bacillus anthracis arid nonsylvatic savannahs, B. cereus biovar (Bcbva) sylvatic rainforests. Bcbva-caused anthrax has been implicated as much 38% mortality rainforest ecosystems, where insects enhance the transmission anthrax-causing bacteria. While well-characterized mammals, its points to an unidentified anthrax-resistance mechanism vectors. In secreted toxin component, 83 kDa Protective Antigen (PA83), binds cell-surface receptors cleaved furin into evolutionary-conserved PA20 pore-forming PA63 subunits. We show that increases resistance Drosophila flies Culex mosquitoes bacterial challenges, without directly affecting growth. further PA83 loop known release from is, part, responsible for PA20-mediated protection. found Toll activating peptidoglycan-recognition protein-SA (PGRP-SA) Toll/NF-κB pathway necessary protection infected flies. This effect on innate immunity may also exist mammals: we human PGRP-SA ortholog. Moreover, constitutive activity Imd/NF-κB MAPKK Dsor1 mutant sufficient confer infections manner independent treatment. Lastly, Clostridium septicum alpha protects bacteria, showing other pathogens help resist anthrax. The direct implications insect-mediated wildlife management, with potential applications, such reducing sensitivity pollinating pathogens.