Functional Aspects of Serum and Salivary Antibodies to Candida

There have been many attempts to identify functional activity of serum or salivary antibodies in vitro and in addition some conclusions can be drawn from in vivo models. (Table 3.4) Thus Holmes et al. (2002) showed that while whole saliva promoted the binding of C. albicans to epithelial cell lines, human Candida-specific IgA antibodies could inhibit the adhesion. These antibodies could be absorbed by both Candida or by an anti-IgA. These findings seem to suggest that IgA in the human oral cavity could be functional. This concept is reinforced by the observation that saliva also promotes the adhesion of C. albicans to polystyrene and that salivary IgA antibodies inhibited this adhesion (San-Millan et al., 2000) and the mechanism appeared to be blockage of the adhesins in the cell wall. Interestingly, these authors reported that while saliva increased the adhesion of whole cells of C. albicans to polystyrene, they inhibited the germinated cells, suggesting that function of antibodies may differentiate between the different forms of Candida and thus might be different in the various forms of oral candidiasis. In contrast, Sweet et al. (1995), using human desquamated buccal epithelial cells, showed that binding of Candida was inhibited by saliva and that this inhibition did not appear to be related to the antibody content.

There is evidence that antibodies may be capable of anti-Candida function without the presence of cells. Thus it has been shown that recombinant anti-idiotypic antibodies representing the internal image of a yeast killer toxin could be microbicidal in vitro against Candida (Conti et al., 2002) (Table 3.4). Antibodies have been used in vivo in humans and Tollemar et al. (1999) used a bovine antibody against Candida in bone marrow transplant patients. Repeated oral treatment resulted in a reduction of the colonisation in seven out of ten patients.

There is a suggestion that B cells and therefore antibodies may be more protective against systemic candidiasis than oral can-didiasis. In a B cell knockout mouse model the mice remained resistant to mucosal infection with Candida but significantly more susceptible to systemic candidiasis (Wagner et al., 1996). Oral immunisation with whole cells of Candida has been shown to result in increased resistance to oral can-didiasis (van Wyk and van der, 1994; Rahman and Challacombe, 1995). While this immunisation has been shown to induce salivary IgA antibodies to Candida, protection could not be ascribed to antibodies since adoptive transfer with both CD4 and in some models CD8 cells could result in protection in the recipient (Rahman and Challacombe, 1995).

There seems to be good evidence that at least monoclonal antibodies to C. albicans can result in inhibition of adherence to epithelial cells (Moragues et al., 2003) and also inhibition to polystyrene and by analogy with the solid surface of dentures (Rodier et al., 2003). Serum IgG antibodies can also exhibit such inhibition of adherence. This raises the possibility that in CAC naturally occurring IgA antibodies or serum transudate of IgG antibodies could play a role in inhibiting adherence to dentures, though this has not been proven. This type of response may be antigen specific since immunisation with C. albicans of mice resulted in antibodies, which were protective and those against the pi-6 glucan were blocking (inhibiting adherence) and protective (Bromuro et al., 2002) (Table 3.4).

5.4. Oral Immunity to Candida in HIV Infection

Although patients with HIV infection may have profound systemic cell-mediated immune deficiencies, mucosal immunity appears to be intact until late in the disease process. Thus, Coogan and Challacombe (2000) showed that salivary IgA antibodies to a 65-kDa heat shock protein were raised in HIV-infected patients compared with controls, and with patients with AIDS. These responses were further raised in the presence of candidiasis. Although CD4+ cells are low in number in HIV-positive individuals, CD8+ cells appear to be the main infiltrate in CHC in either HIV-positive or HIV-negative individuals (Myers et al., 2003). Some authors have found no relationship of salivary antibodies with candidiasis in HIV infection (Wozniak et al., 2002)

whilst others have shown that antibodies to specific Candida antigens such as Saps are related to the amount of colonisation and infection (Millon et al., 2001).

In general, results from HIV suggest that mucosal responses are not impaired until later on in the infection and particularly in AIDS (Challacombe and Sweet, 1997).

5.5. Serum Antibodies-Responses to Oral Candida Infection in Humans

Serum antibodies against whole cell or Candida antigens can be detected in the sera of most persons, given sensitive enough detection techniques. This probably reflects the fact that Candida is a commensal in the mouth and other mucosal surfaces of approximately 40% of the population and also that such antigens are able to stimulate a systemic serum antibody response.

Few studies, however, have attempted to discover whether serum antibodies differ between the four main types of oral Candida infections seen in non-immunocompromised individuals. If it is accepted that CAC is

Table 3.4. Mechanisms Reported for Antibody Activity against Candida

Action

Substrate

Class

Author

Inhibition of adherence

Hep2 cells

Monoclonal

Moragues et al. (2003)

Inhibition of germination

Candida

Monoclonal

Moragues et al. (2003)

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