To investigate the role of B cells and antibody in the immune response of mice to the murine intestinal parasite Giardia muris, we used mice treated from birth with rabbit
anti-IgM antisera (aIgM). 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 (greater than 11 wk) and high trophozoite counts. In contrast, normal, untreated mice or NRS-treated animals developed anti-parasite
IgA and
IgG 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 two strains of mice: BALB/c and (C57BL/6 X 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 first demonstration that
anti-IgM 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.