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Bacillus anthracis lethal toxin reduces human alveolar epithelial barrier function.
The sepsis model: an emerging hypothesis for the lethality of inhalation anthrax.
Resistance of human alveolar macrophages to Bacillus anthracis lethal toxin.
Inflammatory cytokine response to Bacillus anthracis peptidoglycan requires phagocytosis and lysosomal trafficking.
Anti-peptidoglycan antibodies and Fc? receptors are the key mediators of inflammation in Gram-positive sepsis.
Bacillus anthracis peptidoglycan stimulates an inflammatory response in monocytes through the p38 mitogen-activated protein kinase pathway.
Bacillus anthracis spore movement does not require a carrier cell and is not affected by lethal toxin in human lung models.
Neither Lys- and DAP-type peptidoglycans stimulate mouse or human innate immune cells via Toll-like receptor 2.
Anthrax Edema and Lethal Toxins Differentially Target Human Lung and Blood Phagocytes.
Bacillus anthracis spores stimulate cytokine and chemokine innate immune responses in human alveolar macrophages through multiple mitogen-activated protein kinase pathways.
Human lung innate immune response to Bacillus anthracis spore infection.
Gene expression profiling of human alveolar macrophages infected by B. anthracis spores demonstrates TNF-alpha and NF-kappab are key components of the innate immune response to the pathogen.
Gene expression profiling of primary human type I alveolar epithelial cells exposed to Bacillus anthracis spores reveals induction of neutrophil and monocyte chemokines.