Y. enterocolitica translocated Yops impair stimulation of T-cells by antigen presenting cells

Kramer, Uwe; Wiedig, Carolin A.

doi:10.1016/j.imlet.2005.03.002

Cited by 6 publications

(2 citation statements)

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“…However, no structural phage genes were identified, providing no evidence for a functional prophage in this region, at least not in the Houston-1 Seq strain. The corresponding region in B. quintana is shorter in size and contains the yopP gene, which codes for a secreted protein that modulates the host immune response and is located on a 70-kb virulence plasmid in Yersinia pestis (32,40).…”

Section: Discussionmentioning

confidence: 99%

Genome Rearrangements, Deletions, and Amplifications in the Natural Population of Bartonella henselae

et al. 2006

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Cats are the natural host for Bartonella henselae, an opportunistic human pathogen and the agent of cat scratch disease. Here, we have analyzed the natural variation in gene content and genome structure of 38 Bartonella henselae strains isolated from cats and humans by comparative genome hybridizations to microarrays and probe hybridizations to pulsed-field gel electrophoresis (PFGE) blots. The variation in gene content was modest and confined to the prophage and the genomic islands, whereas the PFGE analyses indicated extensive rearrangements across the terminus of replication with breakpoints in areas of the genomic islands. We observed no difference in gene content or structure between feline and human strains. Rather, the results suggest multiple sources of human infection from feline B. henselae strains of diverse genotypes. Additionally, the microarray hybridizations revealed DNA amplification in some strains in the so-called chromosome II-like region. The amplified segments were centered at a position corresponding to a putative phage replication initiation site and increased in size with the duration of cultivation. We hypothesize that the variable gene pool in the B. henselae population plays an important role in the establishment of long-term persistent infection in the natural host by promoting antigenic variation and escape from the host immune response.

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Section: Discussionmentioning

confidence: 99%

Genome Rearrangements, Deletions, and Amplifications in the Natural Population of Bartonella henselae

et al. 2006

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“…It should be noted that most studies on the virulence mechanisms of Yersinia are based on studies with infected macrophages, while research on the interaction of Yersinia and DC (6,15,30,53,55,56,64) is lagging behind. Interaction between murine bone marrow-derived DC (BMDC) and Y. enterocolitica was found recently to entail an array of adverse effects on DC functions (15,64), some of which were not reported in a previous study conducted with human monocyte-derived DC (55).…”

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confidence: 99%

Discordance in the Effects ofYersinia pestison the Dendritic Cell Functions Manifested by Induction of Maturation and Paralysis of Migration

et al. 2006

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The encounter between invading microorganisms and dendritic cells (DC) triggers a series of events which include uptake and degradation of the microorganism, induction of a maturation process, and enhancement of DC migration to the draining lymph nodes. Various pathogens have developed strategies to counteract these events as a measure to evade the host defense. In the present study we found that interaction of the Yersinia pestis EV76 strain with DC has no effect on cell viability and is characterized by compliance with effective maturation, which is manifested by surface display of major histocompatibility complex class II, of costimulatory markers, and of the chemokine receptor CCR7. This is in contrast to maturation inhibition and cell death induction exerted by the related species Yersinia enterocolitica WA O:8. Y. pestis interactions with DC were found, however, to impair functions related to cytoskeleton rearrangement. DC pulsed with Y. pestis failed to adhere to solid surfaces and to migrate toward the chemokine CCL19 in an in vitro transmembrane assay. Both effects were dependent on the presence of the pCD1 virulence plasmid and on a bacterial growth shift to 37°C prior to infection. Moreover, while instillation of a pCD1-cured Y. pestis strain into mouse airways triggered effective transport of alveolar DC to the mediastinal lymph node, instillation of Y. pestis harboring the plasmid failed to do so. Taken together, these results suggest that virulence plasmid-dependent impairment of DC migration is the major mechanism utilized by Y. pestis to subvert DC function.Dendritic cells (DC) play a key role at the interface of innate and adaptive immunity (1,36,49). Interactions between DC and bacterial pathogens are therefore important in determining the outcomes of the infectious processes.DC reside in peripheral epithelial tissues in an immature state, where they serve as sentinels for invading microorganisms. Contact with the microorganism triggers a series of programmed events which begin by pathogen internalization and a concomitant stimulation of pattern recognition receptors such as Toll-like receptors, which subsequently leads to conversion of the immature DC into mature DC. Maturation is marked by a reduction in phagocytic ability, an increase in surface expression of major histocompatibility complex (MHC) class II and costimulatory molecules, and production of proinflammatory cytokines. This occurs together with degradation of the pathogen within the phagosome and presentation of microbial antigens on MHC molecules. Maturation is also characterized by changes in the repertoire of chemokine receptor expression, including the up-regulation of CCR7, which facilitates migration to the local lymph node (20,59). This in turn allows DC to activate T cells in an MHC-specific manner and thus initiate an immune response, before undergoing apoptosis in the lymph node. (8,44).In spite of the differences in pathogenesis, certain mechanisms for evading the host innate immunity are shared by all three Yersinia sp...

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Yop Effector Proteins from Yersinia pseudotuberculosis Impair Dendritic Cell Activation

Tansini

Silva

Santos

et al. 2012

Advances in Yersinia Research

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Y. enterocolitica translocated Yops impair stimulation of T-cells by antigen presenting cells

Cited by 6 publications

References 50 publications

Genome Rearrangements, Deletions, and Amplifications in the Natural Population of Bartonella henselae

Genome Rearrangements, Deletions, and Amplifications in the Natural Population of Bartonella henselae

Discordance in the Effects ofYersinia pestison the Dendritic Cell Functions Manifested by Induction of Maturation and Paralysis of Migration

Yop Effector Proteins from Yersinia pseudotuberculosis Impair Dendritic Cell Activation

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