Tryptophan catabolism is unaffected in chronic granulomatous disease

Ghassan J. Maghzal, Susann Winter, Bettina Wurzer, Beng H. Chong, Rikard Holmdahl and Roland Stocker ()
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Ghassan J. Maghzal: Victor Chang Cardiac Research Institute
Susann Winter: Karolinska Institutet, 171 77 Stockholm, Sweden
Bettina Wurzer: School of Medical Sciences and Bosch Institute, The University of Sydney
Beng H. Chong: Centre for Vascular Research, University of New South Wales
Rikard Holmdahl: Karolinska Institutet, 171 77 Stockholm, Sweden
Roland Stocker: Victor Chang Cardiac Research Institute

Nature, 2014, vol. 514, issue 7523, E16-E17

Abstract: Abstract Arising from L. Romani et al. Nature 451, 211–215 (2008); doi:10.1038/nature06471 Chronic granulomatous disease (CGD) is an inherited disorder of phagocyte function, caused by a genetic defect in NADPH oxidase (NOX2), leading to an impaired ability of leukocytes to produce superoxide ( )1; CGD subjects are susceptible to chronic infections and hyper-inflammation, although the mechanisms remain unclear. Romani et al.2 reported an aberrant inflammatory response to pulmonary aspergillosis as well as sterile Aspergillus fumigatus to be mediated by a defective tryptophan catabolism to kynurenine caused by lack of in CGD mice. Kynurenine is formed by indoleamine 2,3-dioxygenase-1 (IDO1) in a reaction originally reported to depend on (ref. 3). Here we show that NOX2 deficiency does not attenuate IDO1-mediated tryptophan catabolism in human phagocytes and CGD mice with granulomas arising from an inflammatory response to Aspergillus. There is a Reply to this Brief Communications Arising by Romani, L. & Puccetti, P. Nature 514, http://dx.doi.org/10.1038/nature13845 (2014).

Date: 2014
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DOI: 10.1038/nature13844

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