Effects of Trichinella spiralis infection on intestinal pathology in mice lacking interleukin-4 (IL-4) or intestinal trefoil factor (ITF/TFF3).

The nematode Trichinella spiralis induces pathological changes in the small intestine of the host, which are known to be controlled by immune and inflammatory mediators. The detail of this control has still to be completely understood. Mice deficient in interleukin 4 (IL-4) or in intestinal trefoil factor/trefoil family factor 3 (ITF/TFF3) were infected with T.

High resolution mapping of chromosomal regions controlling resistance to gastrointestinal nematode infections in an advanced intercross line of mice.

Fine mapping of quantitative trait loci (QTL) associated with resistance to the gastrointestinal parasite Heligmosomoides polygyrus was achieved on F(6)/F(7) offspring (1076 mice) from resistant (SWR) and susceptible (CBA) mouse strains by selective genotyping (top and bottom 20% selected on total worm count in week 6). Fecal egg counts were recorded at weeks 2, 4, and 6, and the average was also analyzed. Blood packed cell volume in weeks 3 and 6 and five immunological traits (mucosal mast cell protease 1, granuloma score, IgG1 against adult worm, IgG1, and IgE to L4 antigen) were also recorded.

Mapping of chromosomal regions influencing immunological responses to gastrointestinal nematode infections in mice.

This paper reports the results of a genome-wide search for quantitative trait loci (QTL) influencing immunological responses to infection with the gastro-intestinal nematode parasite Heligmosomoides polygyrus in an F2 population created by crossing the resistant SWR and the susceptible CBA inbred mouse strains. Following infections, intestinal granuloma score at post mortem, mucosal mast cell protease 1, and IgE and IgG1 titres were recorded. The susceptible CBA mice had significantly higher IgG1, but significantly lower IgE, mucosal mast cell protease 1 and granuloma scores than SWR mice.

Cellular and serological responses in resistant and susceptible mice exposed to repeated infection with Heligmosomoides polygyrus bakeri.

An experiment was carried out to compare the parasitological and immunological responses of SWR and CBA mice to trickle (repeated) infection with Heligmosomoides polygyrus. Male mice were given 125 L3 once per week and were killed in groups, together with naïve control mice, weekly until week 8. Worm burdens accumulated in CBA, stabilizing in week 5 in excess of 400 worms and remaining high until week 8.

Concurrent infections with Trypanosoma brucei and Nippostrongylus brasiliensis in mice deficient in inducible nitric oxide.

Concurrent infection with Trypanosoma brucei (Tb) delays the normal protective responses of mice to the gastrointestinal parasite Nippostrongylus brasiliensis (Nb). The course of such infections was followed in mice genetically deficient in inducible nitric oxide synthase (INOS) to assess the role of nitric oxide (NO) in this effect. The time course of trypanosome infection in INOS deficient (INOS-/-) mice was similar to that in wild type (WT) and heterozygote (INOS+/-) mice but did not result in NO production.

Chromosomal regions controlling resistance to gastro-intestinal nematode infections in mice.

Quantitative trait loci (QTL) associated with resistance to an intestinal worm in a well-defined murine model are described. These have been identified in an F(2) population derived from resistant (SWR) and susceptible (CBA) parental mouse strains infected with the gastro-intestinal nematode parasite Heligmosomoides polygyrus. Seven QTL located on six chromosomes are described, associated with components of the complex host response and the differential regulation of parasite survival and reproduction.

Nasal immunization with homogenate and peptide antigens induces protective immunity against Trichinella spiralis.

Mice were successfully immunized against the intestinal nematode Trichinella spiralis by intranasal administration of a 30-mer peptide antigen with cholera toxin B. Immunized mice developed antigen-specific serum immunoglobulin G1, intestinal immunoglobulin A, and a type 2-biased cytokine response. Intranasal immunization therefore generates the Th2-mediated responses required for immunity against intestinal parasites.

Helminths.

Helminths affect more than one quarter of the world's population, contributing significantly to socioeconomic problems in developing countries. Control is heavily dependent on chemotherapy, which can be cost-effectively targeted to school-age children, in whom combined drug treatments work well. Drug resistance, however, is a constant threat.