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Defective tryptophan catabolism underlies inflammation in mouse chronic granulomatous disease

Author

Listed:
  • Luigina Romani

    (University of Perugia)

  • Francesca Fallarino

    (University of Perugia)

  • Antonella De Luca

    (University of Perugia)

  • Claudia Montagnoli

    (University of Perugia)

  • Carmen D’Angelo

    (University of Perugia)

  • Teresa Zelante

    (University of Perugia)

  • Carmine Vacca

    (University of Perugia)

  • Francesco Bistoni

    (University of Perugia)

  • Maria C. Fioretti

    (University of Perugia)

  • Ursula Grohmann

    (University of Perugia)

  • Brahm H. Segal

    (Roswell Park Cancer Institute, Buffalo, New York 14263, USA)

  • Paolo Puccetti

    (University of Perugia)

Abstract

Key role for superoxides In chronic granulomatous disease (CGD), phagocytes lack NADPH oxidase activity and are unable to generate superoxide, making sufferers susceptible to recurrent microbial infections. The precise mechanism involved — and the reasons for exaggerated inflammation in CGD — are unclear. Experiments in genetically engineered CGD mice infected with Aspergillus fumigatus, a frequent infection in CGD patients, supports the theory that superoxide-dependent conversion of tryptophan to kynurenine is defective in CGD, compromising antimicrobial resistance, inflammation, and T-cell homeostasis through a single, as yet unknown mechanism. The finding raises the possibility that replacement therapy with natural kynurenines might help control pathologic inflammation and susceptibility to infection in CGD patients.

Suggested Citation

  • Luigina Romani & Francesca Fallarino & Antonella De Luca & Claudia Montagnoli & Carmen D’Angelo & Teresa Zelante & Carmine Vacca & Francesco Bistoni & Maria C. Fioretti & Ursula Grohmann & Brahm H. Se, 2008. "Defective tryptophan catabolism underlies inflammation in mouse chronic granulomatous disease," Nature, Nature, vol. 451(7175), pages 211-215, January.
    • Handle: RePEc:nat:nature:v:451:y:2008:i:7175:d:10.1038_nature06471
    DOI: 10.1038/nature06471
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