MycoBiomDB – Record Details (MyCo_3406)

Biomarker Record Details

Database ID: MyCo_3406
DB IDMyCo_3406
TitleIndinavir-treated Cryptococcus neoformans promotes an efficient antifungal immune response in immunosuppressed hosts
Year2006
PMID16519014
Fungal Diseases involvedCryptococcus neoformans infection
Associated Medical ConditionNone
GenusCryptococcus
Speciesneoformans
OrganismCryptococcus neoformans
Ethical StatementProcedures involving animals and their care were conducted in con- formity with national and international laws and policies.
Site of InfectionNone
Opportunistic invasiveOpportunistic
Sample typeBody fluid
Sample sourceBlood
Host GroupAnimal
Host Common nameMice
Host Scientific nameMus musculus
Biomarker NameIndinavir+IL-12
Biomarker Full NameIndinavir+Interleukin-12
Biomarker TypeDiagnostic
BiomoleculeProtein
Geographical LocationItaly
CohortFemale, 8/10 weeks old, inbred BALB/c mice were obtained from Harlan Nossan Laboratories (Milan, Italy) and housed at the Animal Facilities of the University of Perugia, Perugia, Italy.
Cohort No.None
Age GroupNone
P ValueNone
SensitivityNone
SpecificityNone
Positive Predictive ValueNone
MICNone
Fold ChangeNone
PathwayNone
Disease Introduction MechanismCryptococcus neoformans is the cause of life-threaten-ing opportunistic infections in immunocompromised subjects including AIDS patients. The host defense against this pathogen is mainly mediated by cellular immunity, and cytokines secreted by type-1 Th cells play a central role in the establishment of protective immunity. These mechanisms usually succeed in restricting the infection within the lung by preventing the pathogenic organism from disseminating to the central nervous system, whereas functional abnormal-ities such as defective interleukin (IL)-12 synthesis facilitate the spread of infection.
TechniqueAnalytic
Analysis MethodFlow Cytometry Analysis
ELISA kitsELISA kits (Biosource).
Assay DataNone
Validation Techniques usedFlow Cytometry Analysis, ELISA
Up Regulation Down RegulationIncrease
Sequence DataNone
External LinkNone