http://orcid.org/0000-0003-4214-8022
![Sample our Medicine, Dentistry, Nursing & Allied Health journals, sign in here to start your FREE access for 14 days]({"type":"image" , "src" : "/sda/5944/TOC-Subject-Sample-2021-Medicine-Dentistry-Nursing-Allied-Health.jpg"})
ABSTRACT
Formerly a commensal organism of the mucosal surfaces of most healthy individuals, Candida albicans is an opportunistic pathogen that causes infections ranging from superficial to the more life-threatening disseminated infections, especially in the ever-growing population of vulnerable patients in the hospital setting. In these situations, the fungus takes advantage of its host following a disturbance in the host defense system and/or the mucosal microbiota. Overwhelming evidence suggests that the gastrointestinal tract is the main source of disseminated C. albicans infections. Major risk factors for disseminated candidiasis include damage to the mucosal intestinal barrier, immune dysfunction, and dysbiosis of the resident microbiota. A better understanding of C. albicans’ interaction with the intestinal epithelial barrier will be useful for designing future therapies to avoid systemic candidiasis. In this review, we provide an overview of the current knowledge regarding the mechanisms of pathogenicity that allow the fungus to reach and translocate the gut barrier.
Graphical abstract
Invasion of C. albicans through the intestinal epithelial barrier.
Abbreviation
| Adenosin Triphosphate | = | ATP |
| Adherens Junctions | = | AJs |
| Agglutinin-Like Sequence | = | ALS |
| Anti-Microbial Proteins | = | AMPs |
| B Lymphocytes | = | LB |
| Candidalysin | = | CL |
| c-Jun N-terminal Kinase | = | JNK |
| Dendritic Cells | = | DCs |
| Epithelial Adhesin Protein | = | EAP |
| Epithelial Growth Factor Receptor | = | EGFR |
| E-twenty-six-specific sequence | = | Ets |
| Extent of cell elongation 1 | = | Ece1 |
| Extracellular-signal-Regulated Kinase | = | ERK |
| Follicle-Associated Epithelium | = | FAE |
| GastroIntestinal | = | GI |
| Gastrointestinally-IndUced Transition | = | GUT |
| Glyco-Protein 2 | = | GP2 |
| Gut-Associated Lymphoid Tissue | = | GALT |
| Gut-associated Microbiota | = | GM |
| Heat Shock Protein | = | HSP |
| High-osmolarity glycerol | = | HOG |
| Hyphal wall protein | = | Hwp |
| Hypoxia Inducible Factor | = | HIF |
| Inflammatory Bowel Disease | = | IBD |
| Intestinal Epithelial Cells | = | IECs |
| Intestinal Epithelium | = | IE |
| Isolated Lymphoid Follicles | = | ILF |
| Macrophages | = | Mφ |
| Mannoproteins | = | MPs |
| Mesenteric Lymph Nodes | = | MLNs |
| Microfold cells | = | M cells |
| Mitogen-Activated Protein Kinases | = | MAPK |
| Mucosal Immune System | = | MIS |
| Neutrophil cells | = | PMNs |
| Next Generation Sequencing | = | NGS |
| Nuclear Factor kappa B | = | NFkB |
| Paneth Cells | = | PCs |
| Pathogen Associated Molecular Patterns | = | PAMPs |
| Pattern Recognition Receptors | = | PRRs |
| Peyers’ Patches | = | PPs |
| PhosphoLipoMannan | = | PLM |
| PhosphoPeptidoMannan | = | PPM |
| Reactive Oxygen Species | = | ROS |
| Regenerating Islet-Derived 3 Gamma | = | REG3γ |
| Scanning Electron Microscopy | = | SEM |
| Secreted Aspartyl Proteases | = | SAPs |
| Secretory group IIA PhosphoLipase A2 | = | sPLA2 |
| Secretory Immunoglobulin A | = | sIgA |
| Short-Chain Fatty Acids | = | SCFAs |
| Sub-Epithelial Domes | = | SED |
| T Lymphocytes | = | LT |
| Tight Junctions | = | TJs |
| Trans Epithelial Electrical Resistance | = | TEER |
| Zonula Occludens | = | ZO |
Disclosure of interest
The authors report no conflict of interest