Journal
INFECTION AND IMMUNITY
Volume 68, Issue 4, Pages 2374-2378Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.68.4.2374-2378.2000
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- NIDDK NIH HHS [R01 DK031764, DK31764] Funding Source: Medline
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Chronic granulomatous disease (CGD) is an inherited disorder of the NADPH oxidase in which phagocytes are defective in generating superoxide and downstream microbicidal reactive oxidants, leading to recurrent life-threatening bacterial and fungal infections. Xanthine oxidase (XO) is another enzyme known to produce superoxide in many tissues. Using the p47(phox-/-) mouse model of CGD, we evaluated the residual antibacterial activity of SO. Clearance of Burkholderia cepacia? a major pathogen in CGD, was reduced in p47(phox-/-) mice compared to that in wild-type mice and was further inhibited in p47(phox-/-) mice by pretreatment with the specific XO inhibitor allopurinol. Hepatic B. cepacia burden aas similar in the two genotypes, but allopurinol significantly reduced net hepatic killing and killing efficiency only in p47(phox-/-) mice. Clearance and killing of intravenous Escherichia coli was intact in p47(phox-/-) mice and nas unaffected by pretreatment with allopurinol. Ln CGD, XO mag. contribute to host defense against a subset of reactive oxidant-sensitive pathogens.
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