| DB ID | MyCo_3498 |
| Title | Secreted aspartic protease 2 of Candida albicans inactivates factor H and the macrophage factor H-receptors CR3 (CD11b/CD18) and CR4 (CD11c/CD18) |
| Year | 2015 |
| PMID | 26306739 |
| Fungal Diseases involved | Candidemia |
| Associated Medical Condition | None |
| Genus | Candida |
| Species | albicans |
| Organism | Candida albicans |
| Ethical Statement | The studies were performed with approval of the ResearchEthics Committee of the Medical Faculty of Friedrich SchillerUniversity, Jena (permission number 2268-04/08) and by therespective Hungarian authorities (permission number ETT TUKEB838/PI/12.). Informed consent for the use of blood samples wasobtained according to the Declaration of Helsinki. |
| Site of Infection | None |
| Opportunistic invasive | Opportunistic |
| Sample type | Biopsy |
| Sample source | Cell culture supernatants |
| Host Group | Human |
| Host Common name | Human |
| Host Scientific name | Homo sapiens |
| Biomarker Name | CD18 |
| Biomarker Full Name | Cluster of differentiation 18 |
| Biomarker Type | Diagnostic |
| Biomolecule | Protein |
| Geographical Location | Germany |
| Cohort | MaterialsPurified human FH and the goat FH-specific polyclonal antibodywere purchased from Merck (Schwalbach, Gemany). The anti-CD11b (clone ICRF44), anti-CD11c (clone B-ly6), anti-CD18 (cloneL130) monoclonal antibodies and isotype controls were purchasedfrom BD Biosciences (Heidelberg, Germany). HRP-conjugated rab-bit anti-goat IgG, FITC-conjugated rabbit anti-goat IgG and F(ab’)2fragments of goat anti-mouse IgG were obtained from Dako (Ham-burg, Germany). The cultureTHP-1 macrophages were differentiated from THP-1 monocyticcells (DSMZ, Braunschweig, Germany) by incubation with 10 nMPMA in RPMI 1640 medium (LONZA, Wuppertal, Germany) con-taining 10% FCS (PAA, Cölbe, Germany) for 24 h.Peripheral blood mononuclear cells (PBMC) were isolated byFicoll-Hypaque (GE Healthcare, Freiburg, Germany) density gra-dient separation and erythrocytes were lysed using a hypotonicsalt solution. |
| Cohort No. | None |
| Age Group | None |
| P Value | None |
| Sensitivity | None |
| Specificity | None |
| Positive Predictive Value | None |
| MIC | None |
| Fold Change | None |
| Pathway | None |
| Disease Introduction Mechanism | Candida albicans is an opportunistic fungal pathogen in humansthat is part of the mucosal microflora in the majority of the human population. It can cause a range of superficial and invasive life-threatening infections in individuals with a compromised immunesystem. C. albicans possesses several virulence factors that assistits success to persist and cause infection in the human host. Oneof the virulence traits of C. albicans is the release of proteolyticenzymes, such as secreted aspartyl proteases (Sap), which cleavefluid-phase and extracellular matrix proteins and thus cause tis-sue damage and facilitate infection. Sap2 is a secreted enzymeessential for C. albicans growth in a protein-rich environment thatcleaves peptide bonds between hydrophobic amino acids. Inthe human host, Sap2 cleaves various proteins of the extracellularmatrix, antimicrobial peptides, and the complement componentsC3b, C4b and C5, and contributes to fungal virulence. The complement system is a crucial humoral component ofinnate immunity, which serves the immediate protection againstintruding microorganisms. Beside its role in pathogen elim-ination mediated directly by formation of the lytic terminalcomplement complex C5b-9 or indirectly by opsonization (mainlywith C3b and C4b complement fragments), the complement systemparticipates in the disposal of immune complexes and apoptoticcells, and the modulation of activation of the cellular componentsof the immune system. |
| Technique | Analytic |
| Analysis Method | Flow Cytometry Analysis |
| ELISA kits | Sandwich ELISA kits from ImmunoTools and eBioscience (Frankfurt, Germany) |
| Assay Data | None |
| Validation Techniques used | ELISA, Western blot, Flow cytometry |
| Up Regulation Down Regulation | Decrease |
| Sequence Data | None |
| External Link | None |
