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Cultivation of Heligmosomoides Polygyrus: An Immunomodulatory Nematode Parasite and its Secreted Products
Published on: April 6, 2015
Evidence for genes controlling resistance to Heligmosomoides bakeri on mouse chromosome 1
Harry Noyes1, John Githiori2, Jan E Bradley3
1Institute of Integrative Biology,Biosciences Building,University of Liverpool Crown Street,Liverpool L69 7ZB,UK.
Abstract:
Resistance to infections with Heligmosomoides bakeri is associated with a significant quantitative trait locus (QTL-Hbnr1) on mouse chromosome 1 (MMU1). We exploited recombinant mice, with a segment of MMU1 from susceptible C57Bl/10 mice introgressed onto MMU1 in intermediate responder NOD mice (strains 1094 and 6109). BALB/c (intermediate responder) and C57Bl/6 mice (poor responder) were included as control strains and strain 1098 (B10 alleles on MMU3) as NOD controls. BALB/c mice resisted infection rapidly and C57Bl/6 accumulated heavy worm burdens. Fecal egg counts dropped by weeks 10-11 in strain 1098, but strains 1094 and 6109 continued to produce eggs, harbouring more worms when autopsied (day 77). PubMed search identified 3 genes (Ctla4, Cd28, Icos) as associated with 'Heligmosomoides' in the B10 insert. Single nucleotide polymorphism (SNP) differences in Ctla4 could be responsible for regulatory changes in gene function, and a SNP within a splice site in Cd28 could have an impact on function, but no polymorphisms with predicted effects on function were found in Icos. Therefore, one or more genes encoded in the B10 insert into NOD mice contribute to the response phenotype, narrowing down the search for genes underlying the H. bakeri resistance QTL, and suggest Cd28 and Ctla4 as candidate genes.
Insights
Researchers identified genes on mouse chromosome 1 linked to resistance against Heligmosomoides bakeri infections. This study narrows down candidate genes, suggesting CD28 and CTLA4 play roles in the immune response to this parasite.
Area of Science:
- Immunology
- Genetics
- Parasitology
Background:
- Resistance to Heligmosomoides bakeri infections in mice is influenced by genetic factors.
- A significant quantitative trait locus (QTL-Hbnr1) on mouse chromosome 1 (MMU1) has been associated with this resistance.
Purpose of the Study:
- To investigate the genetic basis of resistance to Heligmosomoides bakeri infections.
- To identify specific genes within the QTL-Hbnr1 region that contribute to the resistance phenotype.
Main Methods:
- Utilized recombinant mice with introgressed segments of mouse chromosome 1 from susceptible C57Bl/10 mice onto an intermediate responder NOD background.
- Included BALB/c and C57Bl/6 mice as control strains.
- Analyzed fecal egg counts and worm burdens at necropsy.
- Performed PubMed searches to identify candidate genes within the introgressed region.
Main Results:
- Recombinant strains (1094 and 6109) showed continued egg production and higher worm burdens compared to control strain 1098.
- Identified three genes (Ctla4, Cd28, Icos) within the introgressed region associated with Heligmosomoides.
- Found single nucleotide polymorphisms (SNPs) in Ctla4 and Cd28 with potential functional impacts, while Icos showed no predicted functional polymorphisms.
Conclusions:
- Genes within the introgressed B10 segment on NOD mice contribute to the Heligmosomoides bakeri resistance phenotype.
- CD28 and CTLA4 are suggested as candidate genes underlying the H. bakeri resistance QTL.
