Defective tryptophan catabolism underlies inflammation in mouse chronic granulomatous disease

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. Segal and Paolo Puccetti ()
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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

Nature, 2008, vol. 451, issue 7175, 211-215

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.

Date: 2008
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DOI: 10.1038/nature06471

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