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IgE enhances clearance of Trichinella spiralis and regulates mast cell responses in mice
S216 Abstracts
IgE Enhances Clearance of Trichinella Spiralis and Regulates Mast Cell Responses in Mice M. Gurish1, P. J. Bryce2, H. Tao1, A. B. Kisselgof2, E. M. Thornton3, H. R. Miller3, D. S. Friend1, H. C. Oettgen2; 1Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, 2Children’s Hospital, Harvard Medical School, Boston, MA, 3University of Edinburgh, Easter Bush, UNITED KINGDOM. RATIONALE: Trichinella spirals infection elicits a vigorous IgE response and pronounced intestinal and splenic mastocytosis. As IgE both activates mast cells (MC) and promotes their survival in culture, we examined its role in MC responses and parasite elimination in T. spiralis-infected mice. METHODS: Wild-type and IgE-/- mice were infected with T. spiralis. Blood and tissue eosinophil counts, mast cell numbers, serum MCP-1, gut worm expulsion and tissue cysts were followed. RESULTS: Wild-type but not IgE-/- mice mounted a strong IgE response. The splenic mastocytosis observed in BALB/c mice following infection was significantly diminished in IgE-/- mice. Similar levels of peripheral blood eosinophilia occurred in both wild-type and IgE deficient animals. Splenic mast cell numbers and serum levels of mouse MCP-1 were lower in IgE-/- animals and they were slower to eliminate the adult worms from the small intestine. The number of T. spiralis larvae present in the skeletal muscle of IgE-/- mice was about twice that in controls and the fraction of larvae that was necrotic was reduced. CONCLUSIONS: We conclude that IgE promotes parasite expulsion from the gut following T. spiralis infection and participates in the response to larval stages of the parasite. Furthermore, our observations support a role for IgE in the regulation of mast cell homeostasis in vivo. Funding: NIH NIAID
760
J ALLERGY CLIN IMMUNOL FEBRUARY 2004
MONDAY
IgE Enhances Clearance of Trichinella Spiralis and Regulates Mast Cell Responses in Mice M. Gurish1, P. J. Bryce2, H. Tao1, A. B. Kisselgof2, E. M. Thornton3, H. R. Miller3, D. S. Friend1, H. C. Oettgen2; 1Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, 2Children’s Hospital, Harvard Medical School, Boston, MA, 3University of Edinburgh, Easter Bush, UNITED KINGDOM. RATIONALE: Trichinella spirals infection elicits a vigorous IgE response and pronounced intestinal and splenic mastocytosis. As IgE both activates mast cells (MC) and promotes their survival in culture, we examined its role in MC responses and parasite elimination in T. spiralis-infected mice. METHODS: Wild-type and IgE-/- mice were infected with T. spiralis. Blood and tissue eosinophil counts, mast cell numbers, serum MCP-1, gut worm expulsion and tissue cysts were followed. RESULTS: Wild-type but not IgE-/- mice mounted a strong IgE response. The splenic mastocytosis observed in BALB/c mice following infection was significantly diminished in IgE-/- mice. Similar levels of peripheral blood eosinophilia occurred in both wild-type and IgE deficient animals. Splenic mast cell numbers and serum levels of mouse MCP-1 were lower in IgE-/- animals and they were slower to eliminate the adult worms from the small intestine. The number of T. spiralis larvae present in the skeletal muscle of IgE-/- mice was about twice that in controls and the fraction of larvae that was necrotic was reduced. CONCLUSIONS: We conclude that IgE promotes parasite expulsion from the gut following T. spiralis infection and participates in the response to larval stages of the parasite. Furthermore, our observations support a role for IgE in the regulation of mast cell homeostasis in vivo. Funding: NIH NIAID
760
J ALLERGY CLIN IMMUNOL FEBRUARY 2004
MONDAY