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- Title
Tryptophan catabolism is unaffected in chronic granulomatous disease.
- Authors
Maghzal, Ghassan J.; Stocker, Roland; Winter, Susann; Holmdahl, Rikard; Wurzer, Bettina; Chong, Beng H.
- Abstract
Arising from L. Romani et al. 451, 211-215 (2008); doi:10.1038/nature06471Chronic 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 (); CGD subjects are susceptible to chronic infections and hyper-inflammation, although the mechanisms remain unclear. Romani et al. 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).
- Subjects
TRYPTOPHAN metabolism; CHRONIC granulomatous disease; PHAGOCYTES; LEUCOCYTES; INFLAMMATION
- Publication
Nature, 2014, Vol 514, Issue 7523, pE16
- ISSN
0028-0836
- Publication type
Article
- DOI
10.1038/nature13844