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Candida albicans is a major cause of fungal nosocomial infections. Host defense against disseminated infections caused by this yeast strongly relies on myeloid cells of the innate immune system. Recently, several breakthroughs have been made that significantly improved our understanding of the role of macrophages during candidiasis and how C. albicans and macrophages interact. Resident tissue macrophages and macrophages derived from monocytes that infiltrate infected tissues are essential for the initiation of the antifungal immune response, as well as elimination of C. albicans from the bloodstream and infected organs. These cells engulf and try to eliminate the invading fungi through specialized mechanisms. Concurrently, C. albicans tries to survive the stresses imposed by the macrophage, acquires nutrients, and can break free from their captive environment. This review focuses on the most recent insights into the strategies of macrophages to eliminate C. albicans and the fungal counterstrategies to overcome these threats.

Candida albicans is a regular member of the intestinal microbiota in the majority of the human population. This underscores C. albicans' adaptation to life in the intestine without inducing competitive interactions with other microbes, or immune responses detrimental to its survival. However, specific conditions such as a dysbalanced microbiome, a suppression of the immune system, and an impaired intestinal barrier can predispose for invasive, mostly nosocomial, C. albicans infections. Colonization of the intestine and translocation through the intestinal barrier are fundamental aspects of the processes preceding life-threatening systemic candidiasis. Insights into C. albicans' commensal lifestyle and translocation can thus help us to understand how patients develop candidiasis, and may provide leads for therapeutic strategies aimed at preventing infection. In this review, we discuss the commensal lifestyle of C. albicans in the intestine, the role of morphology for commensalism, the influence of diet, and the interactions with bacteria of the microbiota.