{"title":"<i>Candida albicans</i> gastrointestinal colonization resistance: a host-microbiome balancing act.","authors":"Derek J Bays, Hannah P Savage","doi":"10.1128/iai.00610-24","DOIUrl":null,"url":null,"abstract":"<p><p>While <i>Candida albicans</i> is a common, commensal yeast colonizing 50%-60% of humans, it has the potential to expand in the gastrointestinal tract and enter the blood stream resulting in invasive candidiasis. Invasive candidiasis carries a mortality approaching 50%, especially in the most vulnerable, immunocompromised population. Antibacterial use causes an increase in <i>C. albicans</i> gastrointestinal colonization, indicating that the colonic microbiota plays a major role in preventing an uncontrolled expansion, a phenomenon known as colonization resistance. Antibacterials, medications, diet, and co-morbid conditions can all alter the microbiome, creating an altered environment known as dysbiosis. Our understanding of the microbiome continues to advance, and there is increasing evidence that the interactions that the microbiome has on the host are vital in maintaining colonization resistance to pathogens including <i>C. albicans</i>. This review will focus on colonization resistance to <i>C. albicans</i> within the gastrointestinal tract. The scope includes the benefits and consequences of <i>C. albicans</i> colonization, interkingdom interactions of the microbiome on <i>C. albicans</i>, microbiome-host interactions and how these modulate <i>C. albicans</i> colonization, and the impact of medications and diet on colonization resistance.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0061024"},"PeriodicalIF":2.8000,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12418750/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Infection and Immunity","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1128/iai.00610-24","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/8/11 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
While Candida albicans is a common, commensal yeast colonizing 50%-60% of humans, it has the potential to expand in the gastrointestinal tract and enter the blood stream resulting in invasive candidiasis. Invasive candidiasis carries a mortality approaching 50%, especially in the most vulnerable, immunocompromised population. Antibacterial use causes an increase in C. albicans gastrointestinal colonization, indicating that the colonic microbiota plays a major role in preventing an uncontrolled expansion, a phenomenon known as colonization resistance. Antibacterials, medications, diet, and co-morbid conditions can all alter the microbiome, creating an altered environment known as dysbiosis. Our understanding of the microbiome continues to advance, and there is increasing evidence that the interactions that the microbiome has on the host are vital in maintaining colonization resistance to pathogens including C. albicans. This review will focus on colonization resistance to C. albicans within the gastrointestinal tract. The scope includes the benefits and consequences of C. albicans colonization, interkingdom interactions of the microbiome on C. albicans, microbiome-host interactions and how these modulate C. albicans colonization, and the impact of medications and diet on colonization resistance.
期刊介绍:
Infection and Immunity (IAI) provides new insights into the interactions between bacterial, fungal and parasitic pathogens and their hosts. Specific areas of interest include mechanisms of molecular pathogenesis, virulence factors, cellular microbiology, experimental models of infection, host resistance or susceptibility, and the generation of innate and adaptive immune responses. IAI also welcomes studies of the microbiome relating to host-pathogen interactions.