A Zychlinsky

Summary

Affiliation: New York University
Country: USA

Publications

  1. ncbi Apoptosis as a proinflammatory event: what can we learn from bacteria-induced cell death?
    A Zychlinsky
    Dept of Microbiology, New York University School of Medicine, NY 10016, USA
    Trends Microbiol 5:201-4. 1997
  2. ncbi Toll-like receptor-2 transduces signals for NF-kappa B activation, apoptosis and reactive oxygen species production
    A O Aliprantis
    Skirball Institute and Department of Microbiology, New York University School of Medicine, New York 10016, USA
    J Endotoxin Res 7:287-91. 2001
  3. ncbi Cell activation and apoptosis by bacterial lipoproteins through toll-like receptor-2
    A O Aliprantis
    Skirball Institute and Department of Microbiology, New York University School of Medicine, 540 First Avenue, New York, NY 10016, USA
    Science 285:736-9. 1999
  4. ncbi In vivo apoptosis in Shigella flexneri infections
    A Zychlinsky
    The Skirball Institute, New York University School of Medicine, New York, New York 10016, USA
    Infect Immun 64:5357-65. 1996
  5. ncbi Tripeptidyl peptidase II promotes maturation of caspase-1 in Shigella flexneri-induced macrophage apoptosis
    H Hilbi
    The Skirball Institute, Department of Microbiology and Kaplan Cancer Center, New York University School of Medicine, New York, New York 10016, USA
    Infect Immun 68:5502-8. 2000
  6. ncbi How bacteria initiate inflammation: aspects of the emerging story
    D Hersh
    Department of Microbiology, The Skirball Institute, New York University School of Medicine, New York, NY 10016, USA
    Curr Opin Microbiol 1:43-8. 1998
  7. ncbi The apoptotic signaling pathway activated by Toll-like receptor-2
    A O Aliprantis
    Skirball Institute and Department of Microbiology, New York University School of Medicine, 540 First Avenue, New York, NY 1001, USA
    EMBO J 19:3325-36. 2000
  8. ncbi The regulatory protein PhoP controls susceptibility to the host inflammatory response in Shigella flexneri
    J E Moss
    Skirball Institute and Department of Microbiology, New York University Medical Center, NY 10016, USA
    Cell Microbiol 2:443-52. 2000
  9. ncbi Release of Toll-like receptor-2-activating bacterial lipoproteins in Shigella flexneri culture supernatants
    A O Aliprantis
    Skirball Institute and Department of Microbiology, New York University School of Medicine, New York, New York 10016, USA
    Infect Immun 69:6248-55. 2001
  10. ncbi A bacterial invasin induces macrophage apoptosis by binding directly to ICE
    Y Chen
    Skirball Institute, Department of Microbiology and Kaplan Cancer Center, New York University School of Medicine, 540 First Avenue, New York, NY 10016, USA
    EMBO J 15:3853-60. 1996

Collaborators

Detail Information

Publications15

  1. ncbi Apoptosis as a proinflammatory event: what can we learn from bacteria-induced cell death?
    A Zychlinsky
    Dept of Microbiology, New York University School of Medicine, NY 10016, USA
    Trends Microbiol 5:201-4. 1997
    ..Bacteria-induced apoptosis appears to promote an inflammatory response that causes tissue damage and further bacterial colonization. Shigella pathogenesis offers a paradigm for the role of apoptosis in bacterial infections...
  2. ncbi Toll-like receptor-2 transduces signals for NF-kappa B activation, apoptosis and reactive oxygen species production
    A O Aliprantis
    Skirball Institute and Department of Microbiology, New York University School of Medicine, New York 10016, USA
    J Endotoxin Res 7:287-91. 2001
    ..We propose that Toll-like receptor-2 fulfils multiple roles in the genesis of the immune response to bacterial pathogens...
  3. ncbi Cell activation and apoptosis by bacterial lipoproteins through toll-like receptor-2
    A O Aliprantis
    Skirball Institute and Department of Microbiology, New York University School of Medicine, 540 First Avenue, New York, NY 10016, USA
    Science 285:736-9. 1999
    ..Thus, hTLR2 is a molecular link between microbial products, apoptosis, and host defense mechanisms...
  4. ncbi In vivo apoptosis in Shigella flexneri infections
    A Zychlinsky
    The Skirball Institute, New York University School of Medicine, New York, New York 10016, USA
    Infect Immun 64:5357-65. 1996
    ..Macrophages, T cells, and B cells are shown to undergo apoptosis in vivo. These results indicate that apoptosis may play a crucial role in the pathogenesis of shigellosis...
  5. ncbi Tripeptidyl peptidase II promotes maturation of caspase-1 in Shigella flexneri-induced macrophage apoptosis
    H Hilbi
    The Skirball Institute, Department of Microbiology and Kaplan Cancer Center, New York University School of Medicine, New York, New York 10016, USA
    Infect Immun 68:5502-8. 2000
    ..TPPII was also found to be involved in apoptosis induced by ATP and the protein kinase inhibitor staurosporine. We propose that TPPII participates in apoptotic pathways...
  6. ncbi How bacteria initiate inflammation: aspects of the emerging story
    D Hersh
    Department of Microbiology, The Skirball Institute, New York University School of Medicine, New York, NY 10016, USA
    Curr Opin Microbiol 1:43-8. 1998
    ..There is therefore much greater diversity in the class of molecules and mechanisms by which bacteria engage the host immune system than previously appreciated...
  7. ncbi The apoptotic signaling pathway activated by Toll-like receptor-2
    A O Aliprantis
    Skirball Institute and Department of Microbiology, New York University School of Medicine, 540 First Avenue, New York, NY 1001, USA
    EMBO J 19:3325-36. 2000
    ..These results indicate that caspase activation is an innate immune response to microbial pathogens, culminating in apoptosis and cytokine production...
  8. ncbi The regulatory protein PhoP controls susceptibility to the host inflammatory response in Shigella flexneri
    J E Moss
    Skirball Institute and Department of Microbiology, New York University Medical Center, NY 10016, USA
    Cell Microbiol 2:443-52. 2000
    ..PhoP appears to regulate Shigella susceptibility to PMNs and antimicrobial molecules that are important for the late stages of infection with this enteric bacterium...
  9. ncbi Release of Toll-like receptor-2-activating bacterial lipoproteins in Shigella flexneri culture supernatants
    A O Aliprantis
    Skirball Institute and Department of Microbiology, New York University School of Medicine, New York, New York 10016, USA
    Infect Immun 69:6248-55. 2001
    ..The activation of apoptosis by BLP shed from S. flexneri is discussed as a novel aspect of the interaction of bacteria with the host...
  10. ncbi A bacterial invasin induces macrophage apoptosis by binding directly to ICE
    Y Chen
    Skirball Institute, Department of Microbiology and Kaplan Cancer Center, New York University School of Medicine, 540 First Avenue, New York, NY 10016, USA
    EMBO J 15:3853-60. 1996
    ..We found that IpaB binds directly to ICE and this enzyme is activated during S. flexneri infection. Furthermore, specific inhibitors of ICE prevented Shigella-induced apoptosis...
  11. ncbi The selC-associated SHI-2 pathogenicity island of Shigella flexneri
    J E Moss
    Skirball Institute, New York University Medical Center, 540 First Avenue, New York, NY 10016, USA
    Mol Microbiol 33:74-83. 1999
    ..flexneri strains tested and parts of the island were also found in other Shigella species. SHI-2 may allow Shigella survival in stressful environments, such as those encountered during infection...
  12. ncbi IpaB, a Shigella flexneri invasin, colocalizes with interleukin-1 beta-converting enzyme in the cytoplasm of macrophages
    K Thirumalai
    The Skirball Institute, New York University School of Medicine, New York 10016, USA
    Infect Immun 65:787-93. 1997
    ..In double-labeling experiments, we show that IpaB and ICE colocalize in the cytoplasm of the macrophage, suggesting that soon after secretion, IpaB binds to ICE to initiate apoptosis and to promote the cleavage of IL-1 beta...
  13. ncbi Pathogenicity islands of Shigella
    M Ingersoll
    Skirball Institute and Department of Microbiology, New York University Medical Center, 540 First Avenue, New York, NY 10016, USA
    Curr Top Microbiol Immunol 264:49-65. 2002
  14. ncbi The Salmonella invasin SipB induces macrophage apoptosis by binding to caspase-1
    D Hersh
    Skirball Institute, Department of Microbiology and Kaplan Cancer Center, New York University School of Medicine, 540 First Avenue, New York, NY 10016, USA
    Proc Natl Acad Sci U S A 96:2396-401. 1999
    ..Taken together, the data demonstrate that SipB functions as an analog of the Shigella invasin IpaB...
  15. ncbi Shigella-induced apoptosis is dependent on caspase-1 which binds to IpaB
    H Hilbi
    Skirball Institute, Department of Microbiology and Kaplan Cancer Center, New York University School of Medicine, New York, New York 10016, USA
    J Biol Chem 273:32895-900. 1998
    ..Taken together these data indicate that Shigella-induced apoptosis is distinct from other forms of apoptosis and seems uniquely dependent on Casp-1...