Chlamydial IFN-γ immune evasion is linked to host infection tropism

DOI Web Site 被引用文献6件
  • David E. Nelson
    Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Disease, National Institutes of Health, Hamilton, MT 59840; Department of Medical Microbiology, University of Manitoba, Winnipeg, MB, Canada R3E 0W3; and Department of Medicine, Indiana University School of Medicine, 545 Barnhill Drive, #435, Indianapolis, IN 46202
  • Dezso P. Virok
    Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Disease, National Institutes of Health, Hamilton, MT 59840; Department of Medical Microbiology, University of Manitoba, Winnipeg, MB, Canada R3E 0W3; and Department of Medicine, Indiana University School of Medicine, 545 Barnhill Drive, #435, Indianapolis, IN 46202
  • Heidi Wood
    Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Disease, National Institutes of Health, Hamilton, MT 59840; Department of Medical Microbiology, University of Manitoba, Winnipeg, MB, Canada R3E 0W3; and Department of Medicine, Indiana University School of Medicine, 545 Barnhill Drive, #435, Indianapolis, IN 46202
  • Christine Roshick
    Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Disease, National Institutes of Health, Hamilton, MT 59840; Department of Medical Microbiology, University of Manitoba, Winnipeg, MB, Canada R3E 0W3; and Department of Medicine, Indiana University School of Medicine, 545 Barnhill Drive, #435, Indianapolis, IN 46202
  • Raymond M. Johnson
    Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Disease, National Institutes of Health, Hamilton, MT 59840; Department of Medical Microbiology, University of Manitoba, Winnipeg, MB, Canada R3E 0W3; and Department of Medicine, Indiana University School of Medicine, 545 Barnhill Drive, #435, Indianapolis, IN 46202
  • William M. Whitmire
    Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Disease, National Institutes of Health, Hamilton, MT 59840; Department of Medical Microbiology, University of Manitoba, Winnipeg, MB, Canada R3E 0W3; and Department of Medicine, Indiana University School of Medicine, 545 Barnhill Drive, #435, Indianapolis, IN 46202
  • Deborah D. Crane
    Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Disease, National Institutes of Health, Hamilton, MT 59840; Department of Medical Microbiology, University of Manitoba, Winnipeg, MB, Canada R3E 0W3; and Department of Medicine, Indiana University School of Medicine, 545 Barnhill Drive, #435, Indianapolis, IN 46202
  • Olivia Steele-Mortimer
    Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Disease, National Institutes of Health, Hamilton, MT 59840; Department of Medical Microbiology, University of Manitoba, Winnipeg, MB, Canada R3E 0W3; and Department of Medicine, Indiana University School of Medicine, 545 Barnhill Drive, #435, Indianapolis, IN 46202
  • Laszlo Kari
    Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Disease, National Institutes of Health, Hamilton, MT 59840; Department of Medical Microbiology, University of Manitoba, Winnipeg, MB, Canada R3E 0W3; and Department of Medicine, Indiana University School of Medicine, 545 Barnhill Drive, #435, Indianapolis, IN 46202
  • Grant McClarty
    Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Disease, National Institutes of Health, Hamilton, MT 59840; Department of Medical Microbiology, University of Manitoba, Winnipeg, MB, Canada R3E 0W3; and Department of Medicine, Indiana University School of Medicine, 545 Barnhill Drive, #435, Indianapolis, IN 46202
  • Harlan D. Caldwell
    Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Disease, National Institutes of Health, Hamilton, MT 59840; Department of Medical Microbiology, University of Manitoba, Winnipeg, MB, Canada R3E 0W3; and Department of Medicine, Indiana University School of Medicine, 545 Barnhill Drive, #435, Indianapolis, IN 46202

書誌事項

公開日
2005-07-14
DOI
  • 10.1073/pnas.0504198102
公開者
Proceedings of the National Academy of Sciences

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説明

<jats:p>Chlamydiae are obligate intracellular pathogens that can exhibit a broad host range in infection tropism despite maintaining near genomic identity. Here, we have investigated the molecular basis for this unique host-pathogen relationship. We show that human and murine chlamydial infection tropism is linked to unique host and pathogen genes that have coevolved in response to host immunity. This intimate host-pathogen niche revolves around a restricted repertoire of host species-specific IFN-γ-mediated effector responses and chlamydial virulence factors capable of inhibiting these effector mechanisms. In human epithelial cells, IFN-γ induces indoleamine 2,3-dioxygenase expression that inhibits chlamydial growth by depleting host tryptophan pools. Human chlamydial strains, but not the mouse strain, avoid this response by the production of tryptophan synthase that rescues them from tryptophan starvation. Conversely, in murine epithelial cells IFN-γ induces expression of p47 GTPases, but not indoleamine 2,3-dioxygenase. One of these p47 GTPases (Iigp1) was shown by small interfering RNA silencing experiments to specifically inhibit human strains, but not the mouse strain. Like human strains and their host cells, the murine strain has coevolved with its murine host by producing a large toxin possessing YopT homology, possibly to circumvent host GTPases. Collectively, our findings show chlamydial host infection tropism is determined by IFN-γ-mediated immunity.</jats:p>

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