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Murine Intestinal Humoral Responses in Chronic Schistosoma mansoni Infections
Author(s) -
CRABTREE J. E.,
PULLAR C. E.,
TREJDOSIEWICZ L. K.,
WILSON R. A.
Publication year - 1992
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1992.tb02869.x
Subject(s) - schistosoma mansoni , biology , immunology , antibody , immune system , isotype , antigen , polyclonal antibodies , immunoglobulin a , humoral immunity , immunoglobulin m , immunoglobulin g , intestinal mucosa , schistosoma , microbiology and biotechnology , schistosomiasis , helminths , monoclonal antibody , medicine
Specific and non‐specific production of immunoglobulins (Ig) by the intestinal mucosa was examined in mice infected with the human blood fluke Schistosoma mansoni. Ileal and colonic mucosal tissue samples were cultured for 2 days, the medium replaced and the culture continued for a further 2 days. Ig concentrations and specific antibodies to soluble schistosome egg antigens in culture supernatants were estimated by isotype‐specific ELISA. Cultured mucosae from control mice produced little IgG, but significant amounts of IgA and IgM on prolonged culture, IgG concentrations were increased in infected animals, mainly in the initial culture period, indicative of systemic, rather than local origins. By contrast, significantly increased local production of IgA and IgM occurred after the start of egg deposition in the intestinal mucosae. Although specific anti‐egg antibodies of the IgG and IgM class were detected, none of the local IgA response was specific for schistosome eggs. We conclude that specific intestinal immune responses to schistosome eggs reflect systemic responses, whereas locally increased IgA production is largely non‐specific. This pattern of response is likely to be related to the prior systemic exposure to schistosome eggs, which results in polyclonal local B‐cell activation, but fails to trigger an antigen‐specific IgA mucosal response.