Aryl hydrocarbon receptor activation fails to alter Cholera toxin-specific fecal IgA secretion after oral immunization in mice.

Abstract

Abstract Secretory IgA plays a critical role in neutralizing enteric toxins and protecting against some intestinal pathogens. In mice, activation of the aryl hydrocarbon receptor (AhR) with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has been shown to suppress antigen-specific systemic IgM and IgG responses, whereas the impact of AhR activation on mucosal IgA responses is less clear. The goal of this study was to determine if TCDD exposure could alter fecal levels of antigen-specific IgA after oral immunization. Female C57Bl/6 mice were administered peanut oil (vehicle) or TCDD (10 μg/Kg, po), and, on the following day, each animal was immunized with whole Cholera toxin (CT, 10 μg, po) with two subsequent immunizations being given at 10 day intervals. Antibody levels were measured by ELISA in fecal extracts each week (normalized to protein) and in serum at termination (week 4). We found that total serum IgA levels were significantly decreased (P < 0.05) in TCDD-treated animals, relative to controls. In contrast, no change in total fecal IgA levels was observed in TCDD-treated mice at any time point measured (weeks 1–4). Interestingly, no change in CT-specific serum IgA levels was observed in TCDD-treated mice, whereas TCDD exposure significantly decreased (P < 0.05) CT-specific serum IgG1 and IgM levels. In Feces, as in serum, no change in CT-specific IgA levels was found in TCDD-treated mice at any time point measured (weeks 3–4). These results suggest that intestinal IgA responses are not adversely impacted by TCDD exposure, an observation that markedly contrasts with the suppression of systemic antibody responses widely seen in animals after TCDD treatment.