Host-parasite relationships between Echinostoma caproni and RAG-2-deficient mice

Abstract

The RAG-2-deficient mouse, a strain of genetically altered mice lacking B- and T-lymphocytes, was used as a host for Echinostoma caproni. In all, 12 male RAG mice were exposed to 25 cysts each, and 12 served as uninfected controls. Mice were necropsied at 2 and 3 weeks postinfection (p.i.). The mean number+/-SE (9.7+/-2.4) of worms recovered from infected mice at 2 weeks p.i. was not significantly different from that recovered at 3 weeks p.i. (6.5+/-2.2). The intestinal circumference of infected RAG mice was significantly greater than that of the controls at 2 and 3 weeks p.i. A significant goblet cell hyperplasia occurred at 2 weeks p.i., but the response was not effective in eliminating worms from the RAG mice. The effect of a high cyst burden was examined by exposure of 8 RAG and 8 ICR mice to 100 cysts each. The body length and area and the oral sucker area of worms grown in RAG mice were significantly greater than those of worms grown in ICR mice. Worm recovery at up to 3 months p.i. was examined in RAG mice exposed to 25 cysts and necropsied every 2 weeks p.i. The mean worm recovery recorded at 2 weeks p.i. was significantly greater than that noted at 12 weeks p.i., at which time worm rejection from the RAG mouse host first occurred. The RAG mouse is a useful host for studies on E. caproni in a murine host that lacks B- and T-lymphocytes.

Foodborne Intestinal Flukes in Southeast Asia

“…In addition, mucins increased by a primary Nippostrongylus brasiliensis infection in the intestine of mice were suggested to be responsible for a rapid expulsion of a challenge infection with E. caproni or E. trivolvis [357]. However, a contradicting result was observed in the RAG-2-deficient mice, a strain of genetically lacking B-and T-lymphocytes, infected with E. caproni; goblet cell hyperplasia was marked in RAG-2-deficient mice but worms survived as they did in normal ICR mice [358].…”

Cd4+ T-cell-dependent Goblet Cell Proliferation and Expulsion of Gymnophalloides seoi from the Intestine of C57bl/6 Mice

“…The immune mechanics may be more complex than previously considered because GC hyperplasia was also observed in recombinase activating gene-2 (RAG-2)-deficient mice lacking T-and B-cells (Frazer et al, 1999). These mice failed to reject E. caproni (Frazer et al, 1999). There have been no reports on the observation of alteration of terminal sugar residues on GC mucins in E. caproni and other echinostome models.…”

“…The involvement of GCs in worm expulsion of E. caproni seemed evident (Fujino, Ichikawa, and Fried, 1998). The immune mechanics may be more complex than previously considered because GC hyperplasia was also observed in recombinase activating gene-2 (RAG-2)-deficient mice lacking T-and B-cells (Frazer et al, 1999). These mice failed to reject E. caproni (Frazer et al, 1999).…”

Immunology and pathology of echinostome infections in the definitive host.

“…These results were confirmed by Fried et al (1997) . In the case of E. caproni , the adult worms collected from RAG-2-deficient mice, a strain genetically altered mice lacking B-and T-lymphocytes, showed greater body areas than those from conventional ICR mice (Frazer et al 1999) .…”

“…This limits the use of immunodeficient mice to study the factors determining worm rejection. However, Frazer et al (1999) compared the characteristics of E. caproni infections in RAG-2-deficient and ICR mice. Although significant goblet cell hyperplasia was detected in the infected vs. noninfected RAG mice, this could not be related to the elimination of the parasite.…”