Delayed hypersensitivity to Candida albicans

Conditions and factors influencing the formation of delayed hypersensitivity (DH) to yeast-like fungi of the species C. albicans under experimental conditions have been studied. The intensity of this reaction has been found to depend on the dose and method used for infecting mice, the time of the test and the qualitative state of fungal cells. As the result of this study, the infectious model of DH to C. albicans has been proposed. This model may be used for the study of the influence of different exogenous and endogenous factors of cell-mediated immune response to candidiasis.     

Phenotypic evaluation to differentiate Candida albicans from Candida dubliniensis

This study evaluated the phenotypic tests used to differentiate Candida albicans from Candida dubliniensis. A total of 55 isolates from vaginal secretions, oral cavity and hemoculture were studied. They were originally identified as C. albicans, based on their morphological and physiological characteristics. These isolates were tested for colony color development on CHROMagar Candida medium, growth at 45 degrees C on Sabouraud Dextrose agar, lipolytic activity on Tween 80 Agar medium and colony morphology and chlamydoconidia formation on Staib agar medium. Of the 55 isolates studied, seven yielded one or more phenotypic characteristics suggestive of Candida dubliniensis. These isolates were tested by PCR with specific primers for Candida dubliniensis and API ID 32. The seven isolates were confirmed as Candida albicans. All of these finding indicate that DNA based tests should be used for definitive identification of Candida dubliniensis.     

In-vitro susceptibility of Candida albicans and Candida stellatoidea to sulfamethoxazole

The susceptibility of organisms of the speciesCandida to sulfamethoxazole were tested in-vitro using the disc sensitivity method.Under specified conditions a zone of growth inhibition surrounding sulfamethoxazole tablet sensi disc was consistently produced in cultures ofCandida albicans, Candida stellatoidea andSaccharomyces cervisiae.Diameters of growth inhibition zone were measured and found to be greatest in cultures ofCandida stellatoidea andSaccharomyces, but growth inhibition inCandida albicans cultures was observed to a lesser degree.The correlation between in vivo pathogenicity of organisms of the speciesCandida, and degree of growth inhibition by sulfamethoxazole sensi disc presents an interesting relationship.     

Adherence of Candida albicans to host cells

Abstract Research devoted to uncovering the mechanisms of adherence of Candida albicans to human tissue is reviewed. The physical aspects of adherence of the fungus to host cells and the biochemical and molecular features, as far as they are known, are discussed. Relevant pre- and post-adherence events in the pathogenesis of disease caused by this fungus are also noted. Putative adhesins and surface receptors of C. albicans for host proteins are discussed in detail.     

Canine mycotic stomatitis due to Candida albicans

Candida albicans, a medically important opportunistic yeast is described as the etiologic agent of stomatitis in dogs. The oral swabs collected from 34 dogs showing symptoms of stomatitis or gingivitis such as anorexia, halitosis, bleeding within the oral cavity, dysphagia, ptyalism (salivation) and submandibular lymphadenopathy were cultured for isolation of the causative agent. C. albicans was isolated from four (11.8%) dogs. The isolates were sensitive to clotrimazole, fluconazole and amphotericin-B but were resistant to nystatin. The routine application of Pal's sunflower seed medium and Narayan stain in microbiological laboratories is highly emphasized. It is recommended that the role of C. albicans, as the etiologic agent of canine stomatitis, should be carefully investigated in various clinical related disorders of dogs as well as in other animals.     

Pathways to acetyl-CoA formation in Candida albicans

The supply of acetyl units from the mitochondrion to the cytosol of Candida albicans appears to be dependent only upon the activity of carnitine acetyltransferase (CAT). The enzyme ATP:citrate lyase (ACL), the major source of acetyl units in oleaginous yeasts, is absent from C. albicans in both the mycelial and yeast forms. There appears to be no other active translocation of acetate or acetyl groups except via the action of carnitine acetyltransferase.     

Chromatin-mediated Candida albicans virulence

Candida albicans is the most prevalent human fungal pathogen. To successfully propagate an infection, this organism relies on the ability to change morphology, express virulence-associated genes and resist DNA damage caused by the host immune system. Many of these events involve chromatin alterations that are crucial for virulence. This review will focus on the studies that have been conducted on how chromatin function affects pathogenicity of C. albicans and other fungi. This article is part of a Special Issue entitled: Histone chaperones and Chromatin assembly.     

Candida albicans biofilm-defective mutants

Biofilm formation plays a key role in the life cycles and subsistence of many microorganisms. For the human fungal pathogen Candida albicans, biofilm development is arguably a virulence trait, because medical implants that serve as biofilm substrates are significant risk factors for infection. The development of C. albicans biofilms in vitro proceeds through an early phase, in which yeast cells populate a substrate, an intermediate phase, in which pseudohyphal and hyphal cell types are produced, and a maturation phase, in which continued cell growth is accompanied by accumulation of an extracellular matrix. Here we report the results of a screen for C. albicans biofilm-defective mutants, in which homozygous insertions in NUP85, MDS3, KEM1, and SUV3 were found to block biofilm development. Confocal microscopic examination suggests that nup85, suv3, and mds3 mutations cause early-phase arrest, whereas the kem1 mutation causes intermediate-phase arrest. All of the mutants are defective in hypha production in several media. Analysis of mixed-biofilm development indicates that all of the mutants are defective in the production of hyphae in the context of a biofilm. Because all of the mutants are defective in the retention of cells in the biofilm, we infer that hyphae provide an adherent scaffold that stabilizes the biofilm structure.     

Candida albicans switches mates

The "asexual" human fungal pathogen Candida albicans has recently been engineered to be able to mate. A paper in the August 9, 2002 issue of Cell shows that mating competence is increased dramatically when mating partners are in a rare switch variant cell type that does not normally occur at body temperature.     

Gluconeogenesis in Candida albicans

According to different metabolic situations in various stages of Candida albicans pathogenesis the regulation of carbohydrate metabolism was investigated. We report the genetic characterization of all major C. albicans gluconeogenic and glyoxylate cycle genes (fructose-1,6-bisphosphatase, PEP carboxykinase, malate synthase and isocitrate lyase) which were isolated after functional complementation of the corresponding Saccharomyces cerevisiae deletion mutants. Remarkably, the regulation of the heterologously expressed C. albicans gluconeogenic and glyoxylate cycle genes was similar to that of the homologous S. cerevisiae genes. A C. albicans DeltaCafbp1 deletion strain failed to utilize non-fermentable carbon sources but hyphal growth was not affected. Our results show that regulation of gluconeogenesis in C. albicans is similar to that of S. cerevisiae and that the current knowledge on how gluconeogenesis is regulated will facilitate the physiological understanding of C. albicans.     

Mechanisms of Candida albicans trafficking to the brain

During hematogenously disseminated disease, Candida albicans infects most organs, including the brain. We discovered that a C. albicans vps51Δ/Δ mutant had significantly increased tropism for the brain in the mouse model of disseminated disease. To investigate the mechanisms of this enhanced trafficking to the brain, we studied the interactions of wild-type C. albicans and the vps51Δ/Δ mutant with brain microvascular endothelial cells in vitro. These studies revealed that C. albicans invasion of brain endothelial cells is mediated by the fungal invasins, Als3 and Ssa1. Als3 binds to the gp96 heat shock protein, which is expressed on the surface of brain endothelial cells, but not human umbilical vein endothelial cells, whereas Ssa1 binds to a brain endothelial cell receptor other than gp96. The vps51Δ/Δ mutant has increased surface expression of Als3, which is a major cause of the increased capacity of this mutant to both invade brain endothelial cells in vitro and traffic to the brain in mice. Therefore, during disseminated disease, C. albicans traffics to and infects the brain by binding to gp96, a unique receptor that is expressed specifically on the surface of brain endothelial cells.     

Antibody response to Candida albicans cell wall antigens

The cell wall of Candida albicans is not only the structure where many essential biological functions reside but is also a significant source of candidal antigens. The major cell wall components that elicit a response from the host immune system are proteins and glycoproteins, the latter being predominantly mannoproteins. Both carbohydrate and protein moieties are able to trigger immune responses. Proteins and glycoproteins exposed at the most external layers of the wall structure are involved in several types of interactions of fungal cells with the exocellular environment. Thus, coating of fungal cells with host antibodies has the potential to profoundly influence the host-parasite interaction by affecting antibody-mediated functions such as opsonin-enhanced phagocytosis and blocking the binding activity of fungal adhesins to host ligands. In this review we examine various members of the protein and glycoprotein fraction of the C. albicans cell wall that elicit an antibody response in vivo. Some of the studies demonstrate that certain cell wall antigens and anti-cell wall antibodies may be the basis for developing specific and sensitive serologic tests for the diagnosis of candidiasis, particularly the disseminated form. In addition, recent studies have focused on the potential of antibodies against the cell wall protein determinants in protecting the host against infection. Hence, a better understanding of the humoral response triggered by the cell wall antigens of C. albicans may provide the basis for the development of (i) effective procedures for the serodiagnosis of disseminated candidiasis, and (ii) novel prophylactic (vaccination) and therapeutic strategies to control this type of infections.     

Adherence of Candida albicans and Candida dubliniensis to buccal and vaginal cells

Twenty-seven Candida albicans strains and 26 Candida dubliniensis strains, isolated from HIV patients, were tested for their adherence to buccal and vaginal epithelial cells. Both species showed important levels of adhesion to buccal and vaginal epithelial cells, although C. albicans showed the highest levels of adhesion. These results suggest that both Candida species are well adapted, in terms of adhesion capability, to the oral and vaginal environment.     

Th17 cells in immunity to Candida albicans

Our understanding of immunity to fungal pathogens has advanced considerably in recent years. Particularly significant have been the parallel discoveries in the C-type lectin receptor family and the Th effector arms of immunity, especially Th17 cells and their signature cytokine, IL-17. Many of these studies have focused on the most common human fungal pathogen, Candida albicans, which is typically a commensal microbe in healthy individuals but causes various disease manifestations in immunocompromised hosts, ranging from mild mucosal infections to lethal disseminated disease. Here, we discuss emerging fundamental discoveries with C.?albicans that have informed our overall molecular understanding of fungal immunity. In particular, we focus on the importance of pattern recognition receptor-mediated fungal recognition and subsequent IL-17 responses in host defense against mucosal candidiasis. In light of these recent advances, we also discuss the implications for anticytokine biologic therapy and vaccine development.     

白念珠菌对宿主的黏附机制

白念珠菌对宿主的黏附是白念珠菌感染过程的关键的第一步,因此阐明白念珠菌对宿主的黏附机制对探索新的方法预防和治疗白念珠菌感染至关重要。近年来,研究者们从白念珠菌的表面结构、黏附素以及黏附相关基因等方面对白念珠菌与宿主的黏附机制进行了大量研究。该文就白念珠菌对宿主的黏附机制进行综述。