Inflammatory Bowel Diseases (IBD) are chronic conditions characterized by inflammation of the gastrointestinal tract that heavily burden daily life, result in surgery or other complications, and disrupt the gut microbiome. How IBD influences gut microbial ecology, especially biogeographic patterns of microbial location, and how the gut microbiota can use diet components and microbial metabolites to mediate disease, are still poorly understood. Many studies on diet and IBD in mice use a chemically induced ulcerative colitis model, despite the availability of an immune-modulated Crohn's Disease model. Interleukin-10-knockout (IL-10-ko) mice on a C57BL/6 background, beginning at age 4 or 7 weeks, were fed either a control diet or one containing 10% (w/w) raw broccoli sprouts which was high in the sprout-sourced anti-inflammatory sulforaphane. Diets began 7 days prior to inoculation with Helicobacter hepaticus, which triggers Crohn's-like symptoms in these immune-impaired mice, and ran for two additional weeks. Key findings of this study suggest that the broccoli sprout diet increases sulforaphane concentration in plasma; decreases weight stagnation, fecal blood, and diarrhea associated with enterocolitis; and increases microbiota richness in the gut, especially in younger mice. Sprout diets resulted in some anatomically specific bacterial communities in younger mice, and reduced the prevalence and abundance of potentially pathogenic or otherwise-commensal bacteria which trigger inflammation in the IL-10 deficient mouse, for example, Escherichia coli and Helicobacter. Overall, the IL-10-ko mouse model is responsive to a raw broccoli sprout diet and represents an opportunity for more diet-host-microbiome research. A diet containing 10% raw broccoli sprouts increased the plasma concentration of the anti-inflammatory compound sulforaphane, and may be protective against negative disease characteristics of Helicobacter-induced enterocolitis in interleukin-10 knockout mice, including weight loss or stagnation, fecal blood, and diarrhea. Younger mice responded more strongly to the diet intervention, and resulted in increased gut bacterial community richness and bacterial community similarity by diet treatment and some anatomical locations in the gut, even in mice with adverse reactions to gut microbiota and a relatively short time in which they had been able to recruit them. To our knowledge, IL-10-ko mice have not previously been used to investigate the interactions of host, microbiota, and broccoli, broccoli sprouts, or broccoli bioactives in resolving symptoms of CD.