title: Host response to Candida albicans bloodstream infection and sepsis.
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.
authors.affiliation: a Septomics Research Center ; Friedrich-Schiller-University and Leibniz-Institute for Natural Product Research and Infection Biology-Hans-Knoell-Institute ; Jena , Germany.
authors.forename: Seána
authors.initials: S
authors.lastname: Duggan
authors.forename: Ines
authors.initials: I
authors.lastname: Leonhardt
authors.forename: Kerstin
authors.initials: K
authors.lastname: Hünniger
authors.forename: Oliver
authors.initials: O
authors.lastname: Kurzai
mesh_terms: D056704:Adaptive Immunity; D000818:Animals; D002176:Candida albicans / Q000276:immunology*; D002177:Candidiasis / Q000276:immunology*; D058365:Candidiasis, Invasive / Q000276:immunology*; D003165:Complement System Proteins / Q000276:immunology; D004195:Disease Models, Animal; D016469:Fungemia / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate; D007694:Killer Cells, Natural / Q000276:immunology; D051379:Mice; D009504:Neutrophils / Q000276:immunology; D018805:Sepsis / Q000276:immunology* / Q000382:microbiology
chemical_list: D003165:Complement System Proteins
keywords: Candida albicans; bloodsteam infection; innate immune response; sepsis