Adherence of Candida albicans to buccal and vaginal epithelial cells: ultrastructural observations

1984 ◽  
Vol 30 (8) ◽  
pp. 1001-1007 ◽  
Author(s):  
Richard A. Calderone ◽  
Nurith Lehrer ◽  
Esther Segal
Keyword(s):  
Candida Albicans ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Surface ◽  
Host Cells ◽  
Yeast Cells ◽  
Dense Matrix ◽  
Epithelial Surface ◽  
Vaginal Epithelial Cells ◽  
Epithelial Cell Surface

The adherence of Candida albicans to human buccal and vaginal epithelial cells was studied by transmission electron microscopy. Adherence to epithelial cells was confirmed by both a radiometric assay as well as direct microscopic examination of stained cell preparations. Ultramicroscopic preparations revealed that yeast cells were closely appressed to epithelial cell surfaces and were often partially enclosed within phagocyticlike invaginations of the epithelial cells. A murine model of vaginitis caused by C. albicans was also used to study adherence to epithelial cells and to follow the course of colonization. Ultramicroscopic preparations of murine vaginal tissue revealed that within 2 h postinfection, yeast cells could be seen adhering to epithelial cells. At 6 h postinfection, hyphae and yeast cells were not only found on the epithelial cell surface but also within the submucosal tissue. When observed on the epithelial cell surface, Candida cells were either attached to host cells, or when infected tissue was stained with ruthenium red, Candida cells were observed on the epithelial surface embedded within an electron-dense matrix. Fungal elements were abundant in the submucosa at 24 h postinfection and were still observed on the epithelial cell surface; all of this was accompanied by an inflammatory response.

Ultrastructure of the in situ adherence of Mobiluncus to vaginal epithelial cells

1988 ◽  
Vol 34 (6) ◽  
pp. 757-766 ◽  
Author(s):  
Jan M. De Boer ◽  
Friso H. F. Plantema
Keyword(s):  
Electron Microscopy ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Surface ◽  
Bacterial Vaginosis ◽  
Vaginal Fluid ◽  
Thin Sections ◽  
Epithelial Cell Surface ◽  
Curved Rods

From patients with bacterial vaginosis motile, anaerobic, comma-shaped bacteria can be isolated, which have recently been placed into the new genus Mobiluncus. In this study, electron microscopy was used to examine the in situ adherence of these motile curved rods to detached epithelial cells (comma cells) in vaginal fluid from two patients with bacterial vaginosis. Thin sections showed that the curved rods attached both directly to the epithelial cell surface and at various distances from it. It is concluded that after initial attachment these motile bacteria can grow at the epithelial cell surface in sessile microcolonies. Ruthenium red staining demonstrated a coating of precipitated glycocalyx material both on the surface of the curved rods and on their flagella. This may indicate that in situ the adherent curved rods were enclosed in a very hydrated matrix of exopolysaccharides. Conspicuous was the ability of the curved rods to attach to the epithelial cell surface via their cell tips. However, in situ no specialized bacterial cell surface structures were seen that might explain this polar attachment. Electron microscopy of pure cultures demonstrated that both Mobiluncus curtisii subsp. curtisii and Mobiluncus mulieris can produce a glycocalyx in vitro.

scholarly journals Adhesion of Tritrichomonas foetus to Bovine Vaginal Epithelial Cells

1999 ◽  
Vol 67 (8) ◽  
pp. 3847-3854 ◽  
Author(s):  
B. N. Singh ◽  
J. J. Lucas ◽  
D. H. Beach ◽  
S. T. Shin ◽  
R. O. Gilbert
Keyword(s):  
Epithelial Cells ◽  
Cell Surface ◽  
Trichomonas Vaginalis ◽  
Host Cells ◽  
Tritrichomonas Foetus ◽  
Trypan Blue Exclusion ◽  
Vaginal Epithelial Cells ◽  
Host Parasite

ABSTRACT An in vitro culture system of bovine vaginal epithelial cells (BVECs) was developed to study the cytopathogenic effects ofTritrichomonas foetus and the role of lipophosphoglycan (LPG)-like cell surface glycoconjugates in adhesion of parasites to host cells. Exposure of BVEC monolayers to T. foetusresulted in extensive damage of monolayers. Host cell disruption was measured quantitatively by a trypan blue exclusion assay and by release of 3H from [3H]thymidine-labeled host cells. Results indicated contact-dependent cytotoxicity of host cells byT. foetus. The cytopathogenic effect was a function ofT. foetus density. Metronidazole- or periodate-treatedT. foetus showed no damage to BVEC monolayers. A related human trichomonad, Trichomonas vaginalis, showed no cytotoxic effects, indicating species-specific host-parasite interactions. A direct binding assay was developed and used to investigate the role of a major cell surface LPG-like molecule in host-parasite adhesion. The results of competition experiments showed that the binding to BVECs was displaceable, was saturable, and yielded a typical binding curve, suggesting that specific receptor-ligand interactions mediate the attachment of T. foetus to BVECs. Progesterone-treated BVECs showed enhanced parasite binding. T. foetus LPG inhibited the binding of T. foetus to BVECs; the LPG from T. vaginalis and a variety of other glycoconjugates did not. These data imply specificity of LPG on host-parasite adhesion. Periodate-treated parasites showed no adherence to host cells, indicating the involvement of carbohydrate containing molecules in the adhesion process.

scholarly journals BgaA acts as an adhesin to mediate attachment of some pneumococcal strains to human epithelial cells

Microbiology ◽  
2011 ◽  
Vol 157 (8) ◽  
pp. 2369-2381 ◽  
Author(s):  
Dominique H. Limoli ◽  
Julie A. Sladek ◽  
Lindsey A. Fuller ◽  
Anirudh K. Singh ◽  
Samantha J. King
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Receptor ◽  
Host Cells ◽  
Bacterial Binding ◽  
Human Epithelial Cells ◽  
Adherence Mechanism ◽  
Epithelial Cell Surface

Streptococcus pneumoniae colonization of the respiratory tract is an essential precursor for pneumococcal disease. To colonize efficiently, bacteria must adhere to the epithelial-cell surface. S. pneumoniae possesses surface-associated exoglycosidases that are capable of sequentially deglycosylating human glycans. Two exoglycosidases, neuraminidase (NanA) and β-galactosidase (BgaA), have previously been shown to contribute to S. pneumoniae adherence to human epithelial cells, as deletion of either of these genes results in reduced adherence. It has been suggested that these enzymes may modulate adherence by cleaving sugars to reveal a receptor on host cells. Pretreatment of epithelial cells with exogenous neuraminidase restores the adherence of a nanA mutant, whereas pretreatment with β-galactosidase does not restore the adherence of a bgaA mutant. These data suggest that BgaA may not function to reveal a receptor, and implicate an alternative role for BgaA in adherence. Here we demonstrate that β-galactosidase activity is not required for BgaA-mediated adherence. Addition of recombinant BgaA (rBgaA) to adherence assays and pretreatment of epithelial cells with rBgaA both significantly reduced the level of adherence of the parental strain, but not the BgaA mutant. One possible explanation of these data is that BgaA is acting as an adhesin and that rBgaA is binding to the receptor, preventing bacterial binding. A bead-binding assay demonstrated that BgaA can bind directly to human epithelial cells, supporting the hypothesis that BgaA is an adhesin. Preliminary characterization of the epithelial-cell receptor suggests that it is a glycan in the context of a glycosphingolipid. To further establish the relevance of this adherence mechanism, we demonstrated that BgaA-mediated adherence contributed to adherence of a recent clinical isolate to primary human epithelial cells. Together, these data suggest a novel role for BgaA as an adhesin and suggest that this mechanism could contribute to adherence of at least some pneumococcal strains in vivo.

scholarly journals Neisseria gonorrhoeae Induces Focal Polymerization of Actin in Primary Human Urethral Epithelium

1998 ◽  
Vol 66 (7) ◽  
pp. 3416-3419 ◽  
Author(s):  
Peter C. Giardina ◽  
Richard Williams ◽  
David Lubaroff ◽  
Michael A. Apicella
Keyword(s):  
Epithelial Cell ◽  
Cell Surface ◽  
Cell Lines ◽  
Conjunctival Epithelium ◽  
Cytoskeletal Reorganization ◽  
Epithelial Surface ◽  
Immortalized Cell Lines ◽  
Epithelial Cell Surface ◽  
Immortalized Cell ◽  
Cytoskeletal Rearrangements

ABSTRACT The pathogenic Neisseria species induce cytoskeletal reorganization in immortalized cell lines. In Chang conjunctival epithelium and T84 intestinal epithelium, focal cytoskeletal rearrangements in which bacteria contacted the epithelial surface were observed. We show that actin footprints are induced in gonococcus-challenged primary urethral epithelium. Moreover, the microbes induced microvillus extension from the epithelial cell surface. Our results indicate that formation of actin footprints is not an artifact of commonly used immortalized cell lines.

scholarly journals Heterogeneous distribution of Candida albicans cell-surface antigens demonstrated with an Als1-specific monoclonal antibody

Microbiology ◽  
2010 ◽  
Vol 156 (12) ◽  
pp. 3645-3659 ◽  
Author(s):  
David A. Coleman ◽  
Soon-Hwan Oh ◽  
Xiaomin Zhao ◽  
Lois L. Hoyer
Keyword(s):  
Candida Albicans ◽  
Cell Surface ◽  
Spatial Localization ◽  
Host Cells ◽  
Yeast Cells ◽  
Cell Surface Antigens ◽  
Heterogeneous Distribution ◽  
Germ Tubes

Despite an abundance of data describing expression of genes in the Candida albicans ALS (agglutinin-like sequence) gene family, little is known about the production of Als proteins on individual cells, their spatial localization or stability. Als proteins are most commonly discussed with respect to function in adhesion of C. albicans to host and abiotic surfaces. Development of a mAb specific for Als1, one of the eight large glycoproteins encoded by the ALS family, provided the opportunity to detect Als1 during growth of yeast and hyphae, both in vitro and in vivo, and to demonstrate the utility of the mAb in blocking C. albicans adhesion to host cells. Although most C. albicans yeast cells in a saturated culture are Als1-negative by indirect immunofluorescence, Als1 is detected on the surface of nearly all cells shortly after transfer into fresh growth medium. Als1 covers the yeast cell surface, with the exception of bud scars. Daughters of the inoculum cells, and sometimes granddaughters, also have detectable Als1, but Als1 is not detectable on cells from subsequent generations. On germ tubes and hyphae, most Als1 is localized proximal to the mother yeast. Once deposited on yeasts or hyphae, Als1 persists long after the culture has reached saturation. Growth stage-dependent production of Als1, coupled with its persistence on the cell surface, results in a heterogeneous population of cells within a C. albicans culture. Anti-Als1 immunolabelling patterns vary depending on the source of the C. albicans cells, with obvious differences between cells recovered from culture and those from a murine model of disseminated candidiasis. Results from this work highlight the temporal parallels for ALS1 expression and Als1 production in yeasts and germ tubes, the specialized spatial localization and persistence of Als1 on the C. albicans cell surface, and the differences in Als1 localization that occur in vitro and in vivo.

scholarly journals Epithelial Cell Innate Response to Candida albicans

2011 ◽  
Vol 23 (1) ◽  
pp. 50-55 ◽  
Author(s):  
J.R. Naglik ◽  
D. Moyes
Keyword(s):  
Candida Albicans ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Fungal Pathogens ◽  
Fungal Diseases ◽  
Lymphoid Cells ◽  
Innate Response ◽  
Epithelial Surface ◽  
Immune Systems ◽  
Pathogenic Microbes

With the advent of treatments and diseases such as AIDS resulting in increasing numbers of patients with suppressed immune systems, fungal diseases are an escalating problem. Candida albicans is the most common of these fungal pathogens, causing infections in many of these patients. It is therefore important to understand how immunity to this fungus is regulated and how it might be manipulated. Although work has been done to identify the receptors, fungal moieties, and responses involved in anti- Candida immunity, most studies have investigated interactions with myeloid or lymphoid cells. Given that the first site of contact of C. albicans with its host is the mucosal epithelial surface, recent studies have begun to focus on interactions of C. albicans with this site. The results are startling yet in retrospect obvious, indicating that epithelial cells play an important role in these interactions, initiating responses and even providing a level of protection. These findings have obvious implications, not just for fungal pathogens, but also for identifying how host organisms can distinguish between commensal and pathogenic microbes. This review highlights some of these recent findings and discusses their importance in the wider context of infection and immunity.

In vitro binding of Candida albicans yeast cells to human fibronectin

1984 ◽  
Vol 30 (2) ◽  
pp. 221-227 ◽  
Author(s):  
Katherine G. Skerl ◽  
Richard A. Calderone ◽  
Esther Segal ◽  
T. Sreevalsan ◽  
W. Michael Scheld
Keyword(s):  
Candida Albicans ◽  
Epithelial Cells ◽  
Mammalian Cells ◽  
Fluorescent Antibody ◽  
In Vitro Assay ◽  
Yeast Cells ◽  
Vitro Assay ◽  
Vaginal Epithelial Cells ◽  
Human Fibronectin

The binding of Candida albicans yeast cells to human fibronectin (Fn), a major glycoprotein of mammalian cells, was studied using an in vitro assay. Adherence was quantitated in microtiter dishes coated with Fn to which radiolabeled yeast cells were added. Under optimum conditions of the assay, i.e., 1 mM CaCl2 and 70 μg Fn protein, approximately 40% of the radiolabeled yeast cells adhered to the Fn. Adherence to Fn was greater at 30 °C than at 4 °C and was greater with viable yeast cells than with heat-killed cells. Candida albicans (two strains) and C. tropicalis adhered to Fn to a greater extent than C. pseudotropicalis, C. krusei, or Saccharomyces cerevisiae. Pretreatment of C. albicans with chymotrypsin, pronase, or papain, but not pepsin, decreased adherence to Fn. Blocking experiments using mannan, sugars, or amino sugars were carried out by preabsorbing the Fn with each of the above-mentioned compounds. Candida mannan blocked adherence of C. albicans to Fn. The mannan effect was dose dependent. However, adherence of C. albicans to Fn was not significantly reduced by mannose, glucose, or several other sugars. The role of FN as a receptor for the binding of C. albicans yeast cells to buccal and vaginal epithelial cells was investigated also using an in vitro assay. We determined, using indirect fluorescent antibody techniques, that both buccal and vaginal epithelial cells possessed Fn. In addition, yeast cells, when pretreated with Fn, showed reduced adherence with buccal and vaginal cells when compared with nontreated cells. These studies may indicate a role for Fn in the adherence of C. albicans to buccal and vaginal epithelial cells.

scholarly journals Vaginal and Oral Epithelial Cell Anti-Candida Activity

2002 ◽  
Vol 70 (12) ◽  
pp. 7081-7088 ◽  
Author(s):  
Fatema Nomanbhoy ◽  
Chad Steele ◽  
Junko Yano ◽  
Paul L. Fidel,
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Surface ◽  
Carbohydrate Moiety ◽  
Sulfated Polysaccharides ◽  
Cell Mediated Immunity ◽  
Oral Epithelial Cell ◽  
Vaginal Epithelial Cells ◽  
Oral Epithelial ◽  
Oral Cells

ABSTRACT Candida albicans is the causative agent of acute and recurrent vulvovaginal candidiasis (VVC), a common mucosal infection affecting significant numbers of women in their reproductive years. While any murine host protective role for cell-mediated immunity (CMI), humoral immunity, and innate resistance by neutrophils against the vaginal infection appear negligible, significant in vitro growth inhibition of Candida species by vaginal and oral epithelial cell-enriched cells has been observed. Both oral and vaginal epithelial cell anti-Candida activity has a strict requirement for cell contact to C. albicans with no role for soluble factors, and oral epithelial cells inhibit C. albicans through a cell surface carbohydrate moiety. The present study further evaluated the inhibitory mechanisms by murine vaginal epithelial cells and the fate of C. albicans by oral and vaginal epithelial cells. Similar to human oral cells, anti-Candida activity produced by murine vaginal epithelial cells is unaffected by enzymatic cleavage of cell surface proteins and lipids but sensitive to periodic acid cleavage of surface carbohydrates. Analysis of specific membrane carbohydrate moieties, however, showed no role for sulfated polysaccharides, sialic acid residues, or glucose and mannose-containing carbohydrates, also similar to oral cells. Staining for live and dead Candida in the coculture with fluorescein diacetate (FDA) and propidium iodide (PI), respectively, showed a clear predominance of live organisms, suggesting a static rather than cidal action. Together, the results suggest that oral and vaginal epithelial cells retard or arrest the growth rather than kill C. albicans through an as-yet-unidentified carbohydrate moiety in a noninflammatory manner.

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