C albicanshost Cell Interaction from the Host Point of View

A number of studies have utilised host DNA microarrays to examine transcriptional changes occurring when host cells interact with C. albicans or with C. albicans-derived cell wall components (Huang et al., 2001; Ishibashi et al., 2004; McLaren et al., 2004; Mullick et al., 2004; Barker et al., 2005; Kim et al., 2005; Fradin et al., 2006). These studies have been performed for a human monocytic cell line (Barker et al., 2005), blood cells (Ishibashi et al., 2004; McLaren et al., 2004; Kim et al., 2005; Fradin et al., 2006), cell line-derived granulocytes (Mullick et al., 2004), and dendritic cells (Huang et al., 2001). Unsurprisingly, for the monocytic cell line, PBMCs, granulocytes and dendritic cells, upregulation of genes involved in the pro-inflammatory response occurred, including TNFA (encodes TNF-a), MIP1A and MIP1B (encoding macrophage inflammatory proteins), and IL1B (encoding IL1-ß) (Huang et al., 2001; Mullick et al., 2004; Barker et al., 2005; Kim et al., 2005; Fradin et al., 2006). These studies define the transcript profile of monocytic cells in the early response to C. albicans (Barker et al., 2005), and demonstrated regulation of genes over several hours of interaction (Kim et al., 2005). In addition, it was shown that C. albicans also induced genes associated with apoptosis in granulocytic cells (Mullick et al., 2004). Therefore, C. albicans is not only an inducer of genes involved in recruitment and activation of neutrophils and mono-cytes, but also affects genes involved in cell survival. The expression profile of neutrophils suggested that transcription was not required to attack and kill microbes, although interaction with C. albicans did induce expression of genes associated with immune cell communication (Fradin et al., 2006).

Proteomics have also been used to examine changes in the proteome occurring when macrophages are infected by C. albicans (Shin et al., 2005; Shin et al., 2006). The most prominent changes were to glycolytic enzymes, proteins involved in cell integrity and in nitric oxide production (Shin et al., 2005). Galectin-3 was also found to be significantly downregulated in infected macrophages (Shin et al., 2006). As binding to galectin-3 directly induces death of C. albicans (Kohatsu et al., 2006), this may represent a method of evading the immune system.

Transcript profiling has also shown that PBMCs differentially respond to soluble and particulate glucans from C. albicans (Ishibashi et al., 2004). Although common genes were regulated by the two glucans (many encoding proinflammatory mole cules), glucan-specific transcription patterns were also noted. It is suggested that the different glucans stimulate different biological activities via differing activation mechanisms (Ishibashi et al., 2004).

One of the major findings from transcript profiling experiments was that the transcript profile obtained for the whole population of PBMC was not reflective of the major cells in the population, the CD4+ or CD8+ lymphocytes (McLaren et al., 2004). This suggests that results obtained for transcript profiling cannot always be extrapolated to the whole population. Transcript profiling has also demonstrated that dendritic cells have pathogen-specific transcript profiles, as well as a core response, suggested to produce pathogen-specific responses (Huang et al., 2001).

Cure Your Yeast Infection For Good

Cure Your Yeast Infection For Good

The term vaginitis is one that is applied to any inflammation or infection of the vagina, and there are many different conditions that are categorized together under this ‘broad’ heading, including bacterial vaginosis, trichomoniasis and non-infectious vaginitis.

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