THE EXPULSION OF ECHINOSTOMA-TRIVOLVIS CAUSED BY GOBLET CELL HYPERPLASIA IN SEVERE COMBINED IMMUNODEFICIENT (SCID) MICE

Mice with severe combined immunodeficiency (SCID), lacking functional T and B lymphocytes, were each infected with 40 Echinostoma trivolvis metacercarial cysts on day 0. The mice of the test group were given in tramuscular injections of dexamethasone (DEX) daily for 2 weeks and ne cropsied on days 5, 8, 12, 15, 20 and 30 post-infection (p. i.). The c ontrol mice, not treated with DEX, were each infected with 40 echinost ome cysts on day 0 and necropsied on the some days as the DEX-treated mice. In the control mice, worm rejection began about day 8 p. i. and the worms were completely rejected by day 15 p. i., corresponding io t he peak in goblet cell hyperplasia, about day 12 p. i. In the DEX-trea ted mice, goblet cell hyperplasia was significantly suppressed and the worms were retained until day 15 p. i., and then rejected after the l ast treatment with DEX. The number of mucosal mast cells, that increas ed with worm infection and peaked about day 15 p, i., was apparently s uppressed by treatment with DEX. The eosinophil number in the controls increased on day 15 p. i. approximately and then decreased. The eosin ophil number in the DEX-treated mice increased as in the controls, but was significantly suppressed compared to that of the controls during the period of the experiment. Enzyme-linked immunosorbent assay [ELISA ] showed no marked rise in titres of the sera IgM, IgA and IgG through out the experiment in both groups. These results indicate that DEX-tre atment delayed the rejection of E. trivolvis from the smell intestine of SCID mice in association with the suppression of goblet cell hyperp lasia it is concluded that the host immune system is not involved in t he rejection of E. trivolvis and the effector cells far worm rejection are goblet cells that markedly increase in numbers by infection with E. trivolvis.