Adaptive Response of Yersinia Pestis to Extracellular Effectors of Innate Immunity During Bubonic Plague
Adaptive response of Yersinia pestis to extracellular effectors of innate immunity during bubonic plague Florent Sebbane*†, Nadine Lemaıˆtre*‡§, Daniel E. Sturdevant¶, Roberto Rebeil*ʈ, Kimmo Virtaneva¶, Stephen F. Porcella¶, and B. Joseph Hinnebusch*,** *Laboratory of Zoonotic Pathogens and ¶Genomics Core Facility, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840; ‡Institut National de la Sante´et de la Recherche Me´dicale Unite´801 and Faculte´deMe´ decine Henri Warembourg, Universite´de Lille II, Lille F-59045, France; and §Institut Pasteur, Lille F-59021, France Edited by John J. Mekalanos, Harvard Medical School, Boston, MA, and approved June 13, 2006 (received for review February 11, 2006) Yersinia pestis causes bubonic plague, characterized by an en- phagocytic oxidative burst that generates antimicrobial reactive larged, painful lymph node, termed a bubo, that develops after oxygen species (ROS), down-regulate the normal proinflamma- bacterial dissemination from a fleabite site. In susceptible animals, tory response, and induce apoptosis of dendritic cells, NK cells, the bacteria rapidly escape containment in the lymph node, spread macrophages, and polymorphonuclear neutrophils (PMNs) (3, 4, systemically through the blood, and produce fatal sepsis. The 6–8). Although substantial, most of the experimental evidence fulminant progression of disease has been largely ascribed to the for these models comes from in vitro studies with the less virulent ability of Y. pestis to avoid phagocytosis and exposure to antimi- enteric pathogens Yersinia pseudotuberculosis and Yersinia en- crobial effectors of innate immunity. In vivo microarray analysis of terocolitica or from studies using attenuated strains of Y.
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