C57Bl/6J mice are more energy efficient during parasitic nematode infection, which may explain their ability to tolerate the infection. SWR/J mice, on the other hand, require an increase in food intake to maintain energy stores during nematode infection. In addition, a strong T helper cell 2-mediated immune response that facilitates a prompt clearance of nematode infection in SWR/J mice may have evolved to conserve energy in this strain.

Our aim was to elucidate the contribution of mucosal mast cells to the effector phase of a secondary immune response to Trichinella spiralis. During secondary infection, rats expel 90–99% of T. spiralis first-stage larvae from the intestine in a matter of hours. This phenomenon appears to be unique to rats and has been called rapid expulsion. Primary intestinal infection by T. spiralis induces mastocytosis, and mast cell degranulation occurs when challenged rats exhibit rapid expulsion. These observations have engendered the view that mast cells mediate rapid expulsion. In this study, we report that. immunization of adult Albino Oxford rats by an infection limited to the muscle phase did not induce intestinal mastocytosis, yet such rats exhibited rapid expulsion when challenged orally. Although mastocytosis was absent, the protease unique to mucosal mast cells, rat mast cell protease II (RMCPII), was detected in sera at the time of expulsion. We further evaluated mast cell activity in neonatal rats that display rapid expulsion. Pups born to infected dams displayed rapid expulsion, and RMCPII was detected in their sera. By feeding pups parasite-specific mAbs or polyclonal Abs before challenge infection, it was possible to dissociate mast cell degranulation from parasite expulsion. These results indicate that rapid expulsion can occur in the absence of either intestinal mastocytosis or RMCPII release. Furthermore, release of RMCPII is not sufficient to cause expulsion. The data argue against a role for mast cells in the mechanism underlying the effector phase of protective immunity against T. spiralis in rats.

Summary Intestinal infection with the parasitic nematode, Trichinella spiralis, provides a robust context for the study of mucosal mast cell function. In rats, mucosal mast cells are exposed to parasites during the earliest stage of infection, affording an opportunity for mast cells to contribute to an innate response to infection. During secondary infection, degranulation of rat mucosal mast cells coincides with expulsion of challenge larvae from the intestine. The goal of this study was to evaluate rat bone marrow-derived mast cells (BMMC) and the rat basophilic leukemia cell line (RBL-2H3) as models for mucosal mast cells, using parasite glycoproteins and antibody reagents that have been tested extensively in rats in vivo. We found that BMMC displayed a more robust mucosal phenotype. Although T. spiralis glycoproteins bound to mast cell surfaces in the absence of antibodies, they did not stimulate degranulation, nor did they inhibit degranulation triggered by immune complexes. Parasite glycoproteins complexed with specific monoclonal IgGs provoked release of RMCPII and β-hexosaminidase from both cell types in a manner that replicated results observed previously in passively immunized rats. Our results document that RBL-2H3 cells and BMMC model rat mucosal mast cells in the contexts of innate and adaptive responses to T. spiralis.

Maternal IgE is exclusively transferred to the neonatal foal via colostrum after birth. The primary contact site for maternal IgE is the foal's gut tissue. Our goal was to investigate neonatal tissues for the presence of mucosal mast cells (MCs), and to test whether intestinal neonatal MCs can bind maternal IgE. Tissues from the small intestine, mesenteric and peripheral lymph nodes were harvested immediately after birth (before colostrum uptake), and on days 5, 9 and 36 from healthy neonates. Mucosal MCs were detected using Alcian blue staining. At birth, most MCs were found in the crypt areas of the small intestine. On days 5 and 9, only a few mucosal MCs could be detected. On day 36, many MCs were found in the submucosa. Mucosal MCs were observed in the T‐cell areas of lymph nodes at all time points. To investigate whether intestinal MCs can bind maternal IgE directly after birth, MCs were isolated from the mucosa of the jejunum. The cells were cultured in the presence of fluorochrome conjugated IgE and measured by flow cytometry. Two populations of IgE+ cells were detected. First, an IgEhigh+/MHC class II− population; and second, cells of a IgE+/MHC class II+ phenotype. We concluded that intestinal mucosal MCs express IgE receptors to rapidly bind maternal IgE from ingested colostrum.