Avigdor Shafferman

Ofer Cohen10
Erez Bar-Haim10
Emanuelle Mamroud8
Ayelet Zauberman8
Avital Tidhar8
10Ofer Cohen
10Erez Bar-Haim
8Emanuelle Mamroud
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  • Ayelet Zauberman, Avital Tidhar, Yinon Levy, Erez Bar-Haim, Gideon Halperin, Yehuda Flashner +3 others
  • 2009
An important virulence strategy evolved by bacterial pathogens to overcome host defenses is the modulation of host cell death. Previous observations have indicated that Yersinia pestis, the causative agent of plague disease, exhibits restricted capacity to induce cell death in macrophages due to ineffective translocation of the type III secretion effector(More)
Yersinia pestis is the causative agent of plague. Previously we have isolated an attenuated Y. pestis transposon insertion mutant in which the pcm gene was disrupted. In the present study, we investigated the expression and the role of pcm locus genes in Y. pestis pathogenesis using a set of isogenic surE, pcm, nlpD and rpoS mutants of the fully virulent(More)
Francisella tularensis, the etiological agent of the inhalation tularemia, multiplies in a variety of cultured mammalian cells. Nevertheless, evidence for its in vivo intracellular residence is less conclusive. Dendritic cells (DC) that are adapted for engulfing bacteria and migration towards lymphatic organs could serve as potential targets for bacterial(More)
BACKGROUND Mycobacterium tuberculosis, the causative agent of tuberculosis (TB), infects approximately 8 million annually culminating in approximately 2 million deaths. Moreover, about one third of the population is latently infected, 10% of which develop disease during lifetime. Current approved prophylactic TB vaccines (BCG and derivatives thereof) are of(More)
BACKGROUND Francisella tularensis is an intercellular bacterium often causing fatal disease when inhaled. Previous reports have underlined the role of cell-mediated immunity and IFNgamma in the host response to Francisella tularensis infection. METHODOLOGY/PRINCIPAL FINDINGS Here we provide evidence for the involvement of IL-17A in host defense to(More)
Pneumonic plague is a fatal disease caused by Yersinia pestis that is associated with a delayed immune response in the lungs. Because neutrophils are the first immune cells recruited to sites of infection, we investigated the mechanisms responsible for their delayed homing to the lung. During the first 24 hr after pulmonary infection with a fully virulent(More)
Bacterial infection of the lungs triggers a swift innate immune response that involves the production of cytokines and chemokines that promote recruitment of immune cells from the bone marrow (BM) into the infected tissue and limit the ability of the pathogen to replicate. Recent in vivo studies of pneumonic plague in animal models indicate that the(More)
The cellular arm of the immune response plays a central role in the defense against intracellular pathogens, such as F. tularensis. To date, whole genome immunoinformatic analyses were limited either to relatively small genomes (e.g. viral) or to preselected subsets of proteins in complex pathogens. Here we present, for the first time, an unbiased bacterial(More)
Deciphering the cellular immunome of a bacterial pathogen is challenging due to the enormous number of putative peptidic determinants. State-of-the-art prediction methods developed in recent years enable to significantly reduce the number of peptides to be screened, yet the number of remaining candidates for experimental evaluation is still in the range of(More)
We report the draft whole-genome sequence of the nonproteolytic Bacillus anthracis V770-NP1-R strain. Compared to those of other B. anthracis strains, the genome exhibits unique mutations in multiple targets potentially affecting proteolytic functions. One of these mutations is a deletion that disrupts the NprR quorum-sensing regulator of the NprA protease.