Department of Medicine, University of Virginia, Amebiasis Research Programme, Medical Research Council (Natal), Department of Medicine, Case Western Reserve University School of Medicine, and the Cleveland Veteran's Affairs Medical Center, Charlottesville, Virginia, Republic of South Africa
Monoclonal antibodies directed against the 260-kD galactose-inhibitable adherence protein (GIAP) of Entamoeba histolytica inhibit binding of amebic trophozoites to purified colonic mucins, suggesting that anti-GIAP secretory immunoglobulin A (sIgA) may have a role in host defense in invasive amebiasis. We determined by enzyme-linked immunosorbent assay (ELISA) whether a salivary anti-GIAP sIgA response was present in patients from the Republic of South Africa with invasive E. histolytica infection. In 13 patients with amebic liver abscess (ALA), salivary anti-GIAP sIgA was significantly higher (mean ± SD optical density [OD] = 0.448 ± 0.258) than that determined for seven South African adult patients hospitalized with nonamebic illness (0.084 ± 0.072; P = 0.002), seven healthy South African Adults (0.194 ± 0.119; P = 0.025), and seven healthy adults from Charlottesville, Virginia (0.036 ± 0.023; P = 0.004). Of the patients with ALA, nine had acute disease, and four had been cured of amebiasis 2–8 months previously. There was no significant difference between these two groups in the anti-GIAP sIgA levels. All ALA patients had a high titer serum anti-amebic antibody response, and there was no direct correlation between the level of anti-GIAP salivary IgA and anti-GIAP serum antibodies (R = 0.187). These findings demonstrate that the E. histolytica GIAP is a mucosal antigen in naturally occurring invasive E. histolytica infection.