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Background  Chronic granulomatous disease (CGD) is caused by defects in nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2) complex subunits (gp91  phox   (a.k.a. Nox2), p47  phox  , p67  phox  , p22  phox  , p40  phox  ) leading to reduced phagocyte-derived reactive oxygen species production. Almost half of patients with CGD develop inflammatory bowel disease, and the involvement of the intestinal microbiome in relation to this predisposing immunodeficiency has not been explored.    Results  Although CGD mice do not spontaneously develop colitis, we demonstrate that p47  phox−/−   mice have increased susceptibility to dextran sodium sulfate colitis in association with a distinct colonic transcript and microbiome signature. Neither restoring NOX2 reactive oxygen species production nor normalizing the microbiome using cohoused adult p47  phox−/−   with B6Tac (wild type) mice reversed this phenotype. However, breeding p47  phox+/−   mice and standardizing the microflora between littermate p47  phox−/−   and B6Tac mice from birth significantly reduced dextran sodium sulfate colitis susceptibility in p47  phox−/−   mice. We found similarly decreased colitis susceptibility in littermate p47  phox−/−   and B6Tac mice treated with  Citrobacter rodentium.Conclusions  Our findings suggest that the microbiome signature established at birth may play a bigger role than phagocyte-derived reactive oxygen species in mediating colitis susceptibility in CGD mice. These data further support bacteria-related disease in CGD colitis.    Electronic supplementary material  The online version of this article (doi:10.1186/s40168-016-0159-0) contains supplementary material, which is available to authorized users.

Colitis susceptibility in p47 phox−/− mice is mediated by the microbiome