X-linked immunodeficiency affects the outcome of Schistosoma mansoni infection in the murine model

Abstract

The incidence of the X-linked immunodeficiency (Xid) on the outcome of Schistosoma mansoni infection has been evaluated through a comparative analysis of parasitological and immune parameters in two different mouse strains: control BALB/c and BALB. Xid mice which carry the Xid mutation and lack B1 (CD5+ B) cells. This study clearly demonstrates that infected B1 cell-deficient animals display a higher susceptibility to S. mansoni infection as revealed by an increase in the tissue egg loads and a significantly elevated mortality, as well as an increase in the granuloma densities. The analysis of the humoral and the cellular responses, conducted in the same experimental conditions, indicates differences in terms of cytokine production after specific antigenic stimulation of splenocytes. Larger amounts of IFN-gamma and IL-4 are observed in BALB. Xid mice while IL-10 production is reduced. In parallel, the study of the specific antibody isotype profiles shows higher amounts of specific IgE and IgG1 antibodies and lower amounts of IgM and IgA in BALB. Xid mice. Taken together, these observations support the idea that B cells are playing a role in the ability of mice to tolerate infection with Schistosoma mansoni.

Deficiency of regulatory B cells increases allergic airway inflammation

“…[31][32][33][34] However, the observed increase in IgE in this study is consistent with previous findings in parasite infection models in which Balb.Xid mice produced greater amounts of antigen-specific IgE than control Balb/c mice. [35,36] Levels of several Th2 cytokines were elevated in the lungs of Xid mice compared to control mice following chronic sensitization, suggesting that regulation of pulmonary cytokine levels during chronic asthmatic inflammation may be a normal function of B-1a cells. CRAg stimulation of mediastinal lymph node cells from Xid mice resulted in increased mRNA expression of IL-4, IL-5, IL-10 and IFN-γ.…”

“…Splenocytes from schistosome-infected Balb.Xid mice produced more IFN-γ and IL-4 following specific antigenic challenge in vitro. [36] Balb.Xid mice were also able to resist infection with Leishmania major and produced significantly elevated levels of IFN-γ from lymph node cells following leishmanial antigen stimulation compared to Balb/c control mice. [40] Similarly, resistance to Chagas' disease was reported in Balb.Xid mice along with elevated levels of splenic IL-2, IL-4 and IFN-γ during early stages of infection, and increased susceptibility following anti-IFN-γ treatment of Balb.Xid mice.…”

Tumour-like phenotypes in urothelial cells after exposure to antigens from eggs of Schistosoma haematobium: An oestrogen–DNA adducts mediated pathway?

“…The eggs were hatched and with the resulting miracidia, snails from a susceptible species, Bulinus truncatus strain from Egypt (maintained in our laboratory), were infected. Cercariae were obtained from these snails (Gaubert et al, 1999). Golden hamsters and BALB/c mice were experimentally infected with 100 cercariae; control animals consisted of littermates.…”

Experimental models of Schistosoma mansoni infection

“…1a : Viera & Moraes-Santos (1987); 2: Cheever et al (1987); 2a: Biozzi high (HIII) and low (LIII) responder mice (Blum & Cioli 1978, Catapani et al 1994; 3a: nude athymic mice lacking T cells ; 3b: mice with severe combined immunodeficiency lacking T & B cells (Amiri et al 1992; 3c: mast cell deficient mice (Cheever et al 1987); 3d: Cheever et al (1987); 3e: Gaubert et al (1999); 5a: Yap et al (1977); 5b: β-2 microglobulin deficient mice , Hernandez et al1997b; 5c: mice unable to process class 1 antigens (Yap et al 1977); 5d: receptor for macrophage Inflammatory Protein-1α [CCR-III] (Gao et al 1997); 5e: mice lacking both TNF-α receptors (Yap et al unpublished); 5f: µ-MT mice , Ferru et al 1998) JHD B-less mice had normal granulomas at 8 wk (Hernandez et al 1997a); 5g: Jankovic et al (1997); 5h: Jankovic et al (1998); 5i: IL-4 ko mice from cross of 129J and C57BL/6 mice ; 5j: IL-4 ko mice bred back to the C57BL/6 background (Rosa Brunet et al 1997); 5k: IL-4 ko mice formed using C57BL/6 germline only (Metwali et al 1996);5l: Rosa Brunet et al (1999a); 5m: Wynn et al (1998);5n: Wynn et al (1998);5o: Amiri et al (1994, Yap et al unpublished);5p: (Akihani et al 1996, Rezende et al 1997a, Oliveira et al 2000; 5q: ; 5r: 5 lipoxegenase, 12-lipoxygenase (Secor et al 1998 ↓ / ↓ ? ↑, ↓: increase, decrease or no change; ?…”