Calprotectin is a protein complex consisting of two noncovalently linked peptide chains that are abundantly synthesized by neutrophils, monocytes, certain subpopulations of macrophages, and squamous epithelia, such as oral epithelium and activated epidermal keratinocytes (reviewed in Brandtzaeg et al., 1995). In situ hybridization studies revealed that calprotectin is synthesized in the upper and middle spinous cell layers in the oral mucosa in oral can-didiasis as well as normal tissues, with no clear quantitative differences between infected and uninfected tissues (Eversole et al., 1997). This protein complex is also found in many human body fluids, including saliva (Kleinegger et al., 2001).
Calprotectin has candidastatic activity and inhibits yeast to hyphal transformation (Murthy et al., 1993). The mechanism of the antifungal function of calprotectin is unknown, however it has been suggested that it is based on zinc binding via histidine-containing sequences, which deprives the organism from this essential metal (Sohnle et al., 1991, 2000). In fact, zinc deficiency has a negative effect on C. albicans growth and germination in vitro (Yamaguchi, 1975). The individual peptide calprotectin chains do not exhibit antifungal activity even though they both have zinc-binding capabilities (Sohnle et al., 2000). To explain this finding it was suggested that formation of a stable heterodimer is necessary for maximum zinc affinity (Sohnle et al., 2000). Absence of a requirement for direct contact between calprotectin and the microorganism and reversibility of the antimicrobial activity in the presence of zinc also support zinc scavenging from a distance as a likely mechanism of action (Sohnle et al., 1991).
Although variability in study design and methods make it difficult to compare clinical studies, results comparing salivary calpro-tectin levels in health and oral candidiasis appear to be in conflict with one another. It has been reported that patients with HIV who develop oral candidiasis have significantly lower levels of calprotectin in saliva than those who do not (Muller et al., 1993). On the contrary, two other studies reported higher salivary calprotectin levels associated with higher Candida counts, or presence of oral infection (Kleinegger et al., 2001; Sweet et al., 2001). Inadequate control for confounding factors such as concurrent presence of active periodontal infection, and oral hygiene practices, as well as limited number of subjects examined, may have been the source of these discrepant results. Recently clinical evidence has emerged supporting the notion that salivary calprotectin levels are nonspecifically increased secondary to mucosal inflammation and that HIV infection may negatively affect calprotectin synthesis (Sweet et al., 2001).
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