Salivary lysozyme is a product of the ductal epithelium of major and minor salivary glands, in addition to being potentially synthesized by sPMN. The muramidase activity of lysozyme causing degradation of the murein in bacterial cell walls is mainly responsible for its potent bactericidal activity, which has mostly been characterized for oral streptococci (Laible and Germaine, 1985). Recently, small cationic amphipathic regions were identified in the peptide sequence of lysozyme that exhibited fungicidal activity by inserting into and damaging the fungal cell membrane (During et al., 1999). Exposure of C. albicans oral isolates from HIV-infected patients to physiological concentrations of lysozyme triggered a rapid loss of viability to a variable extent among isolates (Samaranayake et al., 2001).
On a limited number of genotypically defined strains, there was a significant negative correlation between lysozyme resistance and the duration of HIV disease, potentially implying that certain strains of C. albicans may develop progressive resistance over time to innate antifungal defenses such as lysozyme (Samaranayake et al., 2001).
The major sources of lactoferrin in the oral mucosa are the serous cells in salivary glands and the secondary granules of PMN. Although several antimicrobial mechanisms have been identified for lactoferrin, the classical mechanism involves high affinity for iron, which causes inhibition of microbial iron-dependent metabolism (Bellamy et al., 1992). While the iron-binding domain of this molecule is located at the carboxyterminus, the aminoterminus contains a microbicidal peptide sequence, known as lactoferricin (Bellamy et al., 1992). This peptide may be released by enzymatic degradation, which takes place in the gastrointestinal (GI) tract, and is active against fungi like C. albicans (Wakabayashi et al., 1996), although the exact mechanism of its fungicidal activity is still unknown. The fungicidal role of lacto-ferrin in saliva has been questioned by certain investigators since phosphate and bicarbonate ions at physiological salivary concentrations completely blocked its antifungal activity in vitro (Soukka et al., 1992). However, other studies dispute these findings by showing that addition of whole saliva in this in vitro system does not reduce its antifungal activities (Kuipers et al., 2002). As with salivary lysozyme, clinical or animal data supporting a role of lactoferrin in oral candidiasis are lacking.
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