Abstract
Abstract Secretory IgA plays a critical role in neutralizing enteric toxins and protecting against some mucosal pathogens. In mice, activation of the aryl hydrocarbon receptor (AhR) with a single dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has been shown to transiently decrease total fecal IgA levels but increase antigen-specific IgA levels after mucosal antigen challenge. The goal of this study was to determine if TCDD exposure would alter secretion of antigen-specific IgA levels after systemic pathogen challenge. Female C57Bl/6 mice were administered TCDD at 0 or 40 μg/Kg (po) one day prior to infection with Leishmania major promastigotes. Three weeks later, IgA levels were measured by ELISA. L. major-specific IgA levels in serum were readily detected but unchanged by TCDD treatment. L. major-specific lgA was undetected in the feces of any animal. In contrast, total fecal IgA levels (OD) were significantly increased by 34% in TCDD treated animals (p < 0.05). Total spleen and bone marrow cell numbers were reduced significantly in TCDD-treated mice. The expression of IgM heavy chain, IgJ chain, or kappa light chain in these cells (measured by RT-RT-PCR) was unchanged by TCDD treatment. In contrast, the expression of IgA heavy chain was significantly reduced by approximately 50% in TCDD-treated animals. These results suggest that AhR activation enhances bulk IgA secretion but does not enhance secretion of antigen-specific IgA following systemic pathogen challenge.
Published Version
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