This aspect is covered in more detail elsewhere. However, one of the exciting new areas of immunology has been the recognition that epithelial cells play an active part in innate immunity and that epithelial cells can produce factors interactive with the immune system upon contact with bacteria and other antigens. Some of these factors appear to be microbicidal to Candida. For example, Pivarcsi et al. (2003) showed that antimicrobials induced from epithelial cells can kill Candida. This appeared to be dependent on the Candida induction of TLR2 and TLR4 as well as IL-8 expression. Interestingly antibodies against TLR2 or TLR4 blocked both IL-8 and microbicidal activity. TLRs are a novel protein family that recognise conserved motifs called pathogen-associated molecular patterns (PAMPs), which represent broad groups of microbial pathogens or components (bacteria, fungi, RNA, and DNA). Stimulation of TLRs causes an immediate defensive response, including the production of an array of antimicrobial pep-tides and proinflammatory cytokines (through NF-kB), and the expression of cos-timulatory molecules, which are essential for the activation of adaptive immunity. C. albicans can induce immunostimulation through mannan or phospholipomannan recognised by TLR4 (Netea et al., 2002).
Induction of TLR and the interactions with Candida are reviewed elsewhere, but it is clear that this similar interaction with Candida induces soluble factors and that these may play a role in defence of the oral cavity (Netea et al., 2004). It is however established that adherence of Candida to epithelial cells, perhaps stimulated by Saps, result in upregulation of TLR2 and TLR4 in epithelial cells (Roeder et al., 2004).
It is now clear that epithelial cells on stimulation with microbes can produce a number of chemokines and cytokines. The biological relevance of these in vivo is not yet clear. Granulocyte-macrophage colony-stimulating factor (GM-CSF) responses of oral epithelial cells to Candida have been shown to be dependent on contact and are strain and viability dependent (Dongari-Bagtzoglou and Kashleva, 2003). Interestingly these responses are optimal with hyphae rather than yeast forms. Epithelial cells can have direct anti-Candida activity (Nomanbhoy et al., 2002). Such activity appears to require direct contact and is not mediated by soluble factors (Steele et al., 2001). Contact of epithelial cells with Candida can have differential expression of cytokines. Whilst IFN-y is the preferential response of epithelial cells to C.albicans, IL-18 expression was downreg-ulated by the presence of the yeasts (Rouabhia et al., 2002).
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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.