CHRONIC GIARDIA-MURIS INFECTION IN ANTI-IGM-TREATED MICE .1. ANALYSIS OF IMMUNOGLOBULIN AND PARASITE-SPECIFIC ANTIBODY IN NORMAL AND IMMUNOGLOBULIN-DEFICIENT ANIMALS

  • 1 January 1985
    • journal article
    • research article
    • Vol. 134  (6) , 4153-4162
Abstract
To investigate the role of B cells and antibody in the immune response of mice to the murine intestinal parasite G. muris, mice treated from birth with rabbit anti-IgM antisera (aIgM) were used. Such mice developed in serum and in gut secretions extreme Ig deficiency (IgM, IgA, and IgG) relative to control animals. The aIgM-treated mice showed no anti-G. muris antibody in serum or in gut wash material. Infections of G. muris in these mice were chronic, with a high load of parasite present in the small bowel, as reflected by prolonged cyst excretion (> 11 wk) and high trophozoite counts. In contrast, normal, untreated mice or normal rabbit serum-treated animals developed anti-parasite IgA and IgA antibody in serum, demonstrated IgA antibody against the parasite in gut washings, and expelled the parasite within 9 wk. These effects of aIgM treatment on the murine response to primary infection with G. muris were demonstrated in 2 strains of mice: BALB/c and (C57BL/6 .times. C3H/He) F1. It was also observed that the response to G. muris infection in untreated animals was characterized by higher than normal total secretion of IgA into the gut and a concomitant increase in the serum polymeric IgA level. Mice treated with aIgM had a marked decrease of both monomeric and polymeric IgA in serum, and little detectable IgA in the intestinal lumen. These experiments provide the 1st demonstration that aIgM treatment suppresses a specific intestinal antibody response to antigen, and provide evidence that B cells and antibody play a role in the development of an effective response to a primary infection with G. muris in mice.