Immunoglobulin A (IgA), IgA1, and IgA2 antibodies to Candida albicans in whole and parotid saliva in human immunodeficiency virus infection and AIDS

Abstract

Human immunodeficiency virus (HIV)-infected individuals are predisposed to recurrent oral candidiasis, and, although it has been assumed that this is because of deficient mucosal immune responses, this has not been properly established. The present study aimed to compare the concentrations and secretion rates of immunoglobulin A (IgA) and IgA subclass antibodies to Candida albicans in whole and parotid saliva samples from HIV-infected patients, AIDS patients, and control subjects. Levels of IgA antibody to Candida species in whole saliva were higher in the HIV group than in the controls and were highest in the AIDS group (P < 0.05). In parotid saliva, the mean antibody levels were significantly greater in HIV-positive patients than in controls (P < 0.05) but fell to lower levels in the AIDS group. The secretion rates of Candida antibodies in parotid saliva were reduced in AIDS patients compared with HIV patients. The specific activities of the IgA antibodies and both subclasses were significantly higher in the HIV and AIDS patients than in the controls in both whole and parotid saliva (P < 0.05). Antibody levels were significantly correlated with the numbers of Candida organisms isolated from saliva (P < 0.05). These results suggest clear differences in salivary antibody profiles among HIV-infected. AIDS, and control subjects and are indicative of a response to antigenic challenge by infecting Candida species. No obvious defect in the mucosal immune response in the HIV or AIDS groups that might account for the increased prevalence of candidiasis was apparent.

Serum and salivary IgA antibody responses to Saccharomyces cerevisiae, Candida albicans and Streptococcus mutans in orofacial granulomatosis and Crohn's disease

“…Stimulated parotid saliva was collected over 10 min in all patients and controls from the right parotid duct as described previously [19]. Ten of the control subjects and 12 of the patient group showed salivary carriage of C. albicans but all had less than 1500 colony-forming units (cfu)/ml of saliva [20], which was regarded as normal carriage and were therefore not excluded.…”

“…The standard serum was given an arbitrary value of 100 000 units. The mean of the test sample values falling within the range of the standard curve (a minimum of three of the four dilutions was used) was then compared against the standard curve and an antibody concentration determined [20]. A coefficient of variation was calculated for each sample and values in excess of 15% were re-assayed.…”

“…Cross-reactivity of patient sera between the antigens of C. albicans and S. cerevisiae was screened for by a non-competitive absorption protocol. Six high titre samples were absorbed with a one-tenth volume of washed suspension of formalin-fixed C. albicans, S. cerevisiae and S. mutans , respectively, for 1 h at 37 ∞ C and overnight at 4 ∞ C before centrifugation [20]. The serum samples were then assayed in parallel with identical non-absorbed samples for anti-C. albicans , anti-S. cerevisiae or anti-S. mutans activity as described previously and the percentage inhibition calculated.…”

Human immunodeficiency virus type 1 Tat binds to Candida albicans, inducing hyphae but augmenting phagocytosis in vitro

“…48 Furthermore, patients at all stages of HIV infection, compared to uninfected controls, can still mount substantial local immune responses to oral opportunistic infections, such as C. albicans. 49 These ®ndings challenge the view that weakened mucosal immunity alone is responsible for the prevalence of fungal infections in HIV-infected subjects. Deposition of C3d, as well as formation of terminal complement complex (TCC) on the surface of C. albicans (CBS 5982), was determined by¯ow cytometry.…”

Fungal infections associated with HIV infection

“…Whereas organisms must adhere to an oral surface to avoid the flushing action of saliva, host responses are aimed at limiting adherence and colonisation. HIV-infected patients with oral candidiasis produce increased levels of salivary IgA antibodies against C. albicans, which may act to inhibit adhesion (Coogan et al 1994). Salivary mucins may also bind to and inhibit the adherence of C. albicans (Sweet et al 1995).…”