Acquired resistance to Giardia muris in X-linked immunodeficient mice

Abstract

A previous study from this laboratory (D. P. Snider, D. Skea, and B. J. Underdown, Infect. Immun. 56:2838-2842, 1988) indicated that immunodeficient mice expressing the xid gene develop prolonged infections with Giardia muris, unlike immunocompetent mice, which eliminate the intestinal protozoan parasite in 8 to 10 weeks. In this study, CBA/N (xid) and CBA/Ca mice were infected with G. muris cysts and at various times following this primary infection were cured by treatment with metronidazole. In contrast to the marked differences in the ability of xid and normal mice to eliminate a primary infection, mice of both strains were resistant to a secondary challenge of G. muris cysts. These data imply that the mechanism(s) responsible for elimination of a primary infection is not identical to those required to resist a secondary challenge infection. Splenocytes from immunocompetent CBA/Ca mice (but not immunodeficient CBA/N mice) could transfer the ability to eliminate a primary G. muris infection to irradiated mice of either strain. In contrast, splenocytes from previously infected CBA/Ca mice could not transfer resistance to a challenge infection, further supporting the hypothesis that there are differences between mechanisms required to eliminate a primary infection and those necessary to resist a second challenge infection.

Gene polymorphism in transforming growth factor‐beta codon 10 is associated with susceptibility to Giardiasis

“…, 2003). For example, mice with X‐linked immunodeficiency can develop acquired immunity against secondary challenge with G. muris (Skea & Underdown, 1991). These data suggest that B‐cell‐independent host defences against Giardia may play an important role in controlling and clearing infection.…”

Mucosal defences against Giardia

“…In contrast, other reports using animal models have suggested that B cells have only a limited role in anti‐giardial immunity. For example, mice with B cell defects due to X‐linked immunodeficiency can develop acquired immunity against secondary challenge with G. muris (37). A more recent study showed that B cell‐deficient mice infected with either G. lamblia or G. muris controlled infection as well as normal litter‐mate controls after 4 weeks, suggesting that B cells played a limited role, if any, in controlling acute G. lamblia infection in those studies (38).…”

Natural Pathogens of Laboratory Mice, Rats, and Rabbits and Their Effects on Research

“…Protective immunity is dependent upon both cellular and humoral mechanisms (291,522,553), with IFN-␥ somehow playing a role in clearance of trophozoites (685). The mechanisms responsible for elimination of a primary infection may not be identical to those required to resist a secondary challenge infection (600). Reported effects of G. muris include alterations in intestinal disaccharidase levels (142,144) and mucosal immune responses (406), transient reduction in immunoresponsiveness to sheep erythrocytes (43), and increased severity of concurrent infections in athymic (nu/nu) mice (60).…”