Demonstration and partial characterization of parasite-specific immunoglobulin A responses in human strongyloidiasis

By using an enzyme-linked immunosorbent assay, serum immunoglobulin A (IgA) responses directed against Strongyloides stercoralis larvae antigens were measured in 104 presumably immunocompetent individuals with chronic uncomplicated strongyloidiasis and in 15 immunocompromised patients with S. stercoralis infection. Fifty healthy North American adults and 18 patients with other helminthic parasites served as controls. All 50 healthy controls were negative for antibody responses (mean absorbance ± standard deviation = 0.0724 ± 0.040). The mean absorbance of the 18 parasitized controls was 0.230 ± 0.087; two individuals parasitized by Ascaris lumbricoides showed positive antibody responses. The mean absorbance of the immunocompetent patients with strongyloidiasis was 0.680 ± 0.364 with 91 subjects (87.5%) having a positive value (> 0.300). Of the immunocompromised patients (mean absorbance ± standard deviation = 0.735 ± 0.538), 11 (73%) had a positive antibody response test. When the IgA responses of these two groups were compared, they were not significantly different. There were no correlation between the levels of total serum IgA and the concentration of specific IgA in the infected patients. Both IgA and IgG immunoreactive bands were detected on immunoblots of sodium dodecyl sulfate-polyacrylamide gel electrophoresis-separated larval antigen protein blots. Nineteen bands were recognized by IgG, and 13 were recognized by IgA from sera of infected patients. Several bands displayed specific IgG or IgA reactivity. The present work shows that most patients with strongyloidiasis mount specific IgA responses against filariform larval antigens. These responses are, for the most part, directed against antigens that are different from those recognized by IgG. The lack of correlation between the magnitude of the specific serum IgA responses serum and the clinical aspects of the infection suggests that these antibodies may not play a central role in the regulation of this parasitosis.