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Virulence. 2015;6(4):316-26. doi: 10.4161/21505594.2014.988096. Epub 2015 Mar 18.

Host response to Candida albicans bloodstream infection and sepsis.

Author information

1
a Septomics Research Center ; Friedrich-Schiller-University and Leibniz-Institute for Natural Product Research and Infection Biology-Hans-Knoell-Institute ; Jena , Germany.

Abstract

Candida albicans is a major cause of bloodstream infection which may present as sepsis and septic shock - major causes of morbidity and mortality world-wide. After invasion of the pathogen, innate mechanisms govern the early response. Here, we outline the models used to study these mechanisms and summarize our current understanding of innate immune responses during Candida bloodstream infection. This includes protective immunity as well as harmful responses resulting in Candida induced sepsis. Neutrophilic granulocytes are considered principal effector cells conferring protection and recognize C. albicans mainly via complement receptor 3. They possess a range of effector mechanisms, contributing to elimination of the pathogen. Neutrophil activation is closely linked to complement and modulated by activated mononuclear cells. A thorough understanding of these mechanisms will help in creating an individualized approach to patients suffering from systemic candidiasis and aid in optimizing clinical management.

KEYWORDS:

Candida albicans; bloodsteam infection; innate immune response; sepsis

PMID:
25785541
PMCID:
PMC4601378
DOI:
10.4161/21505594.2014.988096
[Indexed for MEDLINE]
Free PMC Article

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