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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A high concentration of yeasts in feces creates the possibility of active penetration of yeast cells into the surrounding tissue and thereby into blood vessels. Fungaemia is probably caused by this process more often than generally suspected. It is our opinion that venous catheters are contaminated very rarely by yeasts residing on the skin and it is more likely that fungaemia is the causative mechanisms. Adhesion of Candida albicans cells to the catheter wall could not be demonstrated in these investigations. The catheter material examined had no fungistatic properties. To prevent catheters becoming a secondary source of infection it would be advisable for manufacturers to add fungistatic substances to the plastic material of venous catheters.
Mycoses 1989 May
PMID:[The significance of central venous catheters in the genesis of Candida endomycoses]. 276 69

Adhesion of microorganisms to various mucosal surfaces appears to be essential for initiating infection. The role of adhesion to host surfaces in pathogenesis of human mycoses, particularly the various manifestations of candidiasis, has been shown experimentally and correlated with epidemiological data.
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PMID:Pathogenesis of human mycoses: role of adhesion to host surfaces. 315

Adhesion and the ability to form filaments are thought to contribute to the pathogenicity of Candida albicans, the leading cause of fungal disease in immunocompromised patients. Int1p is a C. albicans surface protein with limited similarity to vertebrate integrins. INT1 expression in Saccharomyces cerevisiae was sufficient to direct the adhesion of this normally nonadherent yeast to human epithelial cells. Furthermore, disruption of INT1 in C. albicans suppressed hyphal growth, adhesion to epithelial cells, and virulence in mice. Thus, INT1 links adhesion, filamentous growth, and pathogenicity in C. albicans and Int1p may be an attractive target for the development of antifungal therapies.
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PMID:Linkage of adhesion, filamentous growth, and virulence in Candida albicans to a single gene, INT1. 947 96

A non-mycelial strain of wild-type Candida albicans strain 3153 A was produced by repeated subculturing on Sabouraud glucose agar, and maintained on yeast extract-peptone-glucose medium resulting in hydrophobic cells at 26 degrees C and hydrophilic cells at 37 degrees C. The behaviour of cells of this strain was studied in male BALB/c mice, immunocompromised by treatment with cyclophosphamide and cortisone acetate. An ex-vivo assay of cell adherence to tissue sections of liver, spleen, kidney and lymph-nodes was used. The adherence of yeast cells at 26 and 37 degrees C was predominantly produced by hydrophobic cells and was significantly greater in spleen and liver of immunosuppressed mice compared with the organs of control animals. Adhesion was observed in the white and red pulp as well as in the marginal zone of the spleen.
Mycoses 2000
PMID:Adherence in tissues of immunocompromised mice of a non-mycelium producing strain of Candida albicans. 1094 17

Candida albicans cannot only infect skin and mucosa, but can also cause life threatening systemic candidosis. While natural barriers and the immune system of healthy individuals normally prevent such infections, virulence factors exist that enable C. albicans to survive on surfaces and the permit the fungus to invade tissues and organs in immunocompromised patients. Adhesions factors, morphological flexibility and hydrolytic enzymes belong to this group of virulence factors.C.albicans appears to be able to use these specific virulence attributes at distinct stages of an infection or in different types of candidosis. For example, distinct adhension factors are important for the persistence of C. albicans on mucosal epithelial cells, while other factors are necessary for the adhesion to endothelial tissue. The differential expression of specific virulence factors at different stages of an infection could be the reason why C. albicans not only has single genes for extracellular hydrolytic enzymes, but gene families. Both secreted aspartate proteinases (Saps) and secreted lipases (Lips) from C. albicans are encoded by at least 10 different genes. This high number of similar genes might empower C. albicans with the ability to secrete a specific and appropriate enzymatic response at distinct stages of an infection. For both gene families differential expression has been shown in vitro and in vivo, which would be reasonable for such an adaptation. Expression studies revealed that distinct SAP and LIP genes were expressed under conditions when potential subtrates ( proteins or lipids) were not present in the growth medium. Such expression patterns would imply that these genes may have functions other than simply providing nutrients for the fungus. The specific transcription of single SAP genes during the course of an infection suggests that these genes may have specific functions during different stages of an infection. In fact, inhibition studies and the use of mutants with targeted gene disruptions showed that distinct SAP genes (SAP1-3) are important durning infections of skin and mucosa, while others (SAP4-6) are most relevant for systemic infections.
Mycoses 2000
PMID:[Extracellular hydrolytic enzymes and their relevance during Candida albicans infections]. 1129 71

Several recent reports imply the possibility of cariogenicity and periodontal disease linked to denture plaque containing Candida albicans. Adhesion of oral bacteria and Candida species to the extracellular matrix, such as type I collagen, fibronectin and denatured type I collagen, was examined by using adenosine triphosphate (ATP) analysis. The adhesion of C. albicans to intact and denatured type I collagen was significantly greater than those of oral bacteria and other species of Candida. This result suggests that C. albicans possesses the ability to adhere specifically to extracellular matrix, as compared with other Candida species or oral bacteria.
Mycoses 2002 Nov
PMID:Bacterial and Candida adhesion to intact and denatured collagen in vitro. 1242 Dec 87

The pathogenic fungus Paracoccidioides brasiliensis is the causative agent of paracoccidioidomycosis (PCM). This pulmonary mycosis, acquired by inhalation of airborne propagules, may disseminate to several internal organs and tissues, leading to severe disease. Adhesion to host cell components is the first step involved in dissemination of pathogens. Previous studies showed that laminin, the most abundant glycoprotein of the basement membrane, binds to P. brasiliensis yeast cells, enhancing their pathogenicity in the hamster testicle model. As PCM is primarily a pulmonary infection, we studied the influence of previous treatment of yeast cells with laminin on the course of the intratracheal infection of resistant and susceptible mice using high-virulence (Pb18) and low-virulence (Pb265) P. brasiliensis isolates. Laminin treatment did not alter fungal loads, delayed-type hypersensitivity reactions, levels of pulmonary cytokines and production of specific antibodies in any group of Pb18-infected mice. However, early in the infection, a less intense inflammatory reaction was detected in the lungs of the laminin-treated groups. In addition, laminin treatment of Pb265 resulted in a less severe infection as revealed by the lower fungal loads recovered from lungs. Antibody and cytokine levels, however, did not change after laminin treatment. Altogether, our results demonstrate that laminin binding to yeast cells diminishes P. brasiliensis pathogenicity. The lower inflammatory response observed with the virulent isolate and the decreased pulmonary fungal burden with the low-virulence isolate indicate an inhibitory effect of laminin treatment on P. brasiliensis infectivity and interaction with pulmonary host cells or extracellular matrix proteins.
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PMID:Binding of laminin to Paracoccidioides brasiliensis induces a less severe pulmonary paracoccidioidomycosis caused by virulent and low-virulence isolates. 1515 88

The pathogenic fungus Paracoccidioides brasiliensis causes paracoccidioidomycosis, a pulmonary mycosis acquired by inhalation of fungal airborne propagules, which may disseminate to several organs and tissues, leading to a severe form of the disease. Adhesion to and invasion of host cells are essential steps involved in the infection and dissemination of pathogens. Furthermore, pathogens use their surface molecules to bind to host extracellular matrix components to establish infection. Here, we report the characterization of the glyceraldehyde-3-phosphate dehydrogenase (GAPDH) of P. brasiliensis as an adhesin, which can be related to fungus adhesion and invasion. The P. brasiliensis GAPDH was overexpressed in Escherichia coli, and polyclonal antibody against this protein was obtained. By immunoelectron microscopy and Western blot analysis, GAPDH was detected in the cytoplasm and the cell wall of the yeast phase of P. brasiliensis. The recombinant GAPDH was found to bind to fibronectin, laminin, and type I collagen in ligand far-Western blot assays. Of special note, the treatment of P. brasiliensis yeast cells with anti-GAPDH polyclonal antibody and the incubation of pneumocytes with the recombinant protein promoted inhibition of adherence and internalization of P. brasiliensis to those in vitro-cultured cells. These observations indicate that the cell wall-associated form of the GAPDH in P. brasiliensis could be involved in mediating binding of fungal cells to fibronectin, type I collagen, and laminin, thus contributing to the adhesion of the microorganism to host tissues and to the dissemination of infection.
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PMID:Glyceraldehyde-3-phosphate dehydrogenase of Paracoccidioides brasiliensis is a cell surface protein involved in fungal adhesion to extracellular matrix proteins and interaction with cells. 1636 93

Adhesion of Candida species to prosthetic acrylic resins is an essential first step in the pathogenesis of denture stomatitis. Data on the relative adhesion of pathogenic non-albicans Candida species to different denture base materials are sparse. The purpose of the present study was to investigate in vitro adhesion of C. albicans, C. glabrata, C. krusei and C. dubliniensis to four different denture base materials. Specimens of both heat-cured resins (Vertex(TM) Rapid Simplified and ProBase Hot) and cold-cured resins (Paladur A and Paladur B) were prepared using a novel method and the adhesion of four strains each of the foregoing Candida species evaluated microscopically using a soft imaging system. There was a significant difference in yeast adherence between Vertex and the other resins. Only C. glabrata attached to Vertex, while all the remainder of the tested species adhered to all other resins tested except ProBase, which resisted C. krusei adhesion. There was a significant difference in candidal adhesion between cold-cured and heat-cured resins for three Candida species (C. albicans, P = 0.039; C. glabrata, P = 0.002 and C. krusei, P = 0.000). The type of denture base material and whether they are heat-cured or cold-cured play an important role in modifying candidal adhesion.
Mycoses 2006 Mar
PMID:In vitro adhesion of Candida species to denture base materials. 1646 38

Members of the genus Aspergillus are filamentous, ubiquitous fungi found in nature. Aspergillus species can cause clinical settings in man, such as opportunistic infections, allergic states and toxicoses. Immunosuppression is the major factor predisposing to development of opportunistic mycoses. To invade the host, Aspergillus species must be able to adhere to and penetrate the host tissues. Much work has focused on the search for virulence determinants that allow the establishment of the fungus within the host. Adhesins, pigment production, toxic metabolites and extracellular enzymes are thought to be the putative virulence factors of Aspergillus species. Adhesion systems provide binding of conidia to various circulating or basement membrane-associated host proteins; toxic molecules inhibit macrophage phagocytosis and mucociliary action; pigment production aids in longer survival in tissues and also overwhelms the host defence systems; extracellular enzymes degrade the structural barriers in the host. In this review, putative virulence factors of Aspergillus species and their potential role in aspergillosis have been discussed.
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PMID:[Putative virulence factors of Aspergillus species]. 1677 66


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