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Related Experiment Videos

Multiple innate inflammatory responses induced after systemic adenovirus vector delivery depend on a functional

Anne Kiang1, Zachary C Hartman, Ruth S Everett

  • 1Department of Pediatrics, Division of Medical Genetics, Duke University Medical Center, Durham, NC 27710, USA.

Molecular Therapy : the Journal of the American Society of Gene Therapy
|May 31, 2006
PubMed
Summary

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Adenovirus (Ad) triggers inflammation and thrombocytopenia in wild-type mice, but complement deficiency blunts these innate immune responses. Complement system interactions significantly impact Ad-induced inflammation.

Area of Science:

  • Immunology
  • Virology
  • Genetics

Background:

  • Excessive complement activation causes tissue damage and systemic inflammation.
  • Adenovirus (Ad) injections elicit rapid innate immune responses.
  • The role of complement in Ad-induced inflammation is not fully understood.

Purpose of the Study:

  • To investigate the impact of Ad-complement system interactions on Ad-induced innate immune responses.
  • To compare inflammatory responses in complement-deficient versus wild-type mice after Ad injection.

Main Methods:

  • Systemic injection of Ad into C3-knockout (C3-KO) and wild-type (WT) mice.
  • Quantitative comparison of anti-Ad innate immune responses.
  • Analysis of plasma cytokine levels (KC, IL-6, IFN-gamma, etc.) and thrombocytopenia.

Related Experiment Videos

  • Global liver transcriptome analysis using RT-PCR-validated gene arrays.

    • Main Results:

    • WT mice showed rapid increases in multiple inflammatory cytokines and thrombocytopenia post-Ad injection.
    • C3-KO mice exhibited significantly blunted inflammatory responses and avoided Ad-induced thrombocytopenia.
    • Liver transcriptome responses were significantly altered in C3-KO mice compared to WT mice.
    • High-dose Ads effectively transduced hepatocytes in C3-KO mice.

    Conclusions:

    • Adenovirus interactions with the complement system are critical for initiating and exacerbating innate immune responses.
    • Complement activation significantly contributes to Ad-induced inflammation and thrombocytopenia.
    • Complement deficiency does not impede Ad hepatocyte transduction.