The analysis of the adherence capacity of fungi to surfaces of both oral tissue and different tissues would be of interest in the fungal dissemination as an oral and systemic pathogen. We developed an in vitro adenosine triphosphate (ATP)-based assay technique to extract the cellular and fungal ATP separately, which allowed the quantitative evaluation of the adhesion of the yeast to monolayers of human gingival epithelial cells (GEC), gingival fibroblasts (GF) and pulmonary fibroblasts (PF). Seven oral isolates of Candida species (three of Candida albicans, three of Candida tropicalis and one of Candida glabrata) were used in the study. The adherent level of the Candida species varied depending on both the isolates and the cell origins, although all the Candida isolates had a significantly higher level of adherence to GEC than to GF except the single isolate of C. tropicalis. Whereas the adherent level of the five isolates to GEC was significantly higher than that to PF, the adherent level of the remaining two isolates of C. tropicalis to GEC was significantly lower than that to PF. These results suggest that candidal adherence to host tissue cells should be regulated in an isolate-dependent and cell-origin-dependent manner, and that the phenomena may be involved in the colonisation and/or dissemination of the fungi.

The rapid outbreak of the highly pathogenic A/H5N1 avian influenza virus among domestic birds and its transmission to humans have induced worldwide fears of a new influenza pandemic. If a human-trophic strain of A/H5N1 is replicated in domestic animals, it might have high transmissivity and pathogenicity to humans. If the misassembling of both avian and swine influenza viruses occur in the same cells in domestic fowl, novel pandemic infections among humans might emerge due to human-fowl contacts. In the present study, examinations of mixed infections with A/H5N1 and A/H1N1 viruses were carried out using living chickens to elucidate the possibility of chimeric avian-swine influenza virus replication in domestic fowl. The sporadic strains of avian A/H5N1 and swine A/H1N1 viruses were co-infected into embryonated eggs and post-hatched chickens. A double staining method using the anti-A/H5N1 and anti-A/H1N1 antibodies indicated that A/H5N1 and A/H1N1 viruses were co-localized in the same cells in the chorioallantoic membrane of embryos, and in the lungs of chickens challenged by the double infections. This indicated that the avian influenza and swine influenza viruses might be assembling in the same cells of chickens, and chimeric viruses containing the characteristics of both viral strains might appear.

Abstract. SC1 is a cell adhesion molecule that belongs to the immunoglobulin superfamily; this molecule was initially purified from the chick embryonic nervous system and was reported to exhibit homophilic adhesion activity. SC1 is transiently expressed in various organs during development and has been identified in numerous neoplastic tissues, including lung cancer and colorectal carcinomas. The present study focused on the encephalic metastasis of lung cancer cells with respect to the potential function of SC1, as this molecule is known to be consistently expressed in the central nervous system as well as lung cancers. SC1 complementary DNA was introduced into A549 cells, a human lung cancer-derived cell line. The stable overexpression of the SC1 protein in A549 cells was demonstrated to enhance the self-aggregation of the cells. In addition, the SC1 transfectants enhanced the metastatic and invasive potential to the encephalic parenchyma following implantation into nude mice. In conclusion, the results of the present study demonstrated that cell adhesion due interactions between SC1 on brain tissue and SC1 on lung cancer cells was involved in the malignant aspects of lung cancer, including invasion and metastasis to the brain. IntroductionNumerous studies have confirmed that cell adhesion molecules (CAMs) are essential for normal histogenesis as well as tumor malignancies (1-3). In addition, it was reported that dysregulated CAM expression was often involved in certain tumor behavior (4,5). Of note, the inhibition or attenuation of E-cadherin expression in epithelial cells was demonstrated to enhance cellular transformation. A certain CAM, deleted in colorectal cancer (DCC), is a member of the immunoglobulin (Ig) superfamily, which is commonly lost during the development of colorectal tumors. The loss of expression of CAMs, such as DCC, has therefore been suggested to enable the migration and escape of tumor cells from the primary lesion, subsequently resulting in the invasion and the dissemination of metastases. By contrast, various other CAMs have been reported to be overexpressed in numerous types of tumors, which may promote tumor cell invasion and metastasis through their adhesive activities (4,6).SC1 is a cell adhesion molecule that belongs to the Ig superfamily; this molecule was identified in several independent studies, each of which gave it a different title, SC1, bursal epithelium and neurons or DM-general receptor for phosphoinositides 1-associated scaffold protein (7-10). This protein possesses an intracellular domain that carries three C2-type Ig-like motifs followed by two V-type motifs. The homophilic properties of SC1 have been revealed using cellular adhesion experiments on substrates and self-aggregation assays in vitro (8,(11)(12)(13). By contrast, previous studies have also reported heterophilic interactions of SC1, such as that with neuron-glia (Ng)-CAM during the extension of neurites from sympathetic neurons as well as that with CD6 in the hematopoietic system (14,15). SC1 homologs hav...

Gicerin is an immunoglobulin superfamily cell adhesion molecule that plays a role in development via its cell adhesive activities. After maturation, the gicerin expressionalmost disappears in most organs, except for the muscle and endothelial cells. Interestingly, various neoplastic cells strongly express gicerin in their cell membranes, indicating a potential function of gicerin in the development of malignancy. In the present study, we analyzed the potential role of gicerin in the metastasis of melanoma. Gicerin was found to be expressed in the cell membrane of the B16 implantable melanoma cell line. In addition, cell adhesion activity of B16was clearly promoted on gicerin proteins and HUVEC cells, an endothelial cell line. B16 cells were then implanted intravenously into nude mice in order to evaluate the metastatic activity of gicerin in vivo. Following implantation, metastatic lesions were frequently observed in the pulmonary tissues, whereas tumor emboli and extravasation were found in the pulmonary blood vessels. In contrast, no metastatic lesions were detected in the pulmonary tissues of the mice injected with B16 cells preincubated with anti-gicerin polyclonal antibodies. These findings suggest that gicerin enhances the pulmonary metastatic properties of melanoma cells by promoting endothelium-tumor interactions.

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