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Commensal microbes that colonize the intestine are an important cause of invasive infection. However, how colonization of individuals impacts their susceptibility to invasive infection remains undefined. This knowledge gap reflects technical roadblocks in models of long-term commensal colonization by microbes that can also cause invasive infection, and conceptual appreciation for systemic antigen-specific immune modulation primed by commensals. To address this knowledge gap, a model of intestinal colonization with the human commensal and pathogenic fungi, Candida albicans was developed. We show C. albicans intestinal colonization protects against subsequent invasive C. albicans infection. These benefits require tonic stimulation since protection is eliminated in mice eradicated of commensal fungi. Protection against invasive infection parallels the systemic expansion of C. albicans-specific RORγt+ Th17 cells and enhanced IL-17 responsiveness by circulating neutrophils. Reciprocally, the protective benefits of intestinal colonization are overturned by depletion of CD4+ T cells or Ly6G+ neutrophils, or IL-17 neutralization. These results highlight a new facet in the symbiotic relationship between host and microbe in mucosal tissues