Heligmosomoides bakeri: a model for exploring the biology and genetics of resistance to chronic gastrointestinal nematode infections

Abstract

A note on versions:The version presented here may differ from the published version or from the version of record. If you wish to cite this item you are advised to consult the publisher's version. Please see the repository url above for details on accessing the published version and note that access may require a subscription. The intestinal nematode Heligmosomoides bakeri has undergone 2 name changes during the last 4 decades. Originally, the name conferred on the organism in the early 20th century was Nematospiroides dubius, but this was dropped in favour of Heligmosomoides polygyrus, and then more recently H. bakeri, to distinguish it from a closely related parasite commonly found in wood mice in Europe. H. bakeri typically causes long-lasting infections in mice and in this respect it has been an invaluable laboratory model of chronic intestinal nematode infections. Resistance to H. bakeri is a dominant trait and is controlled by genes both within and outside the MHC. More recently, a significant QTL has been identified on chromosome 1, although the identity of the underlying genes is not yet known. Other QTL for resistance traits and for the accompanying immune responses were also defined, indicating that resistance to H. bakeri is a highly polygenic phenomenon. Hence marker-assisted breeding programmes aiming to improve resistance to GI nematodes in breeds of domestic livestock will need to be highly selective, focussing on genes that confer the greatest proportion of overall genetic resistance, whilst leaving livestock well-equipped genetically to cope with other types of pathogens and preserving important production traits.

Cultivation of <em>Heligmosomoides Polygyrus:</em> An Immunomodulatory Nematode Parasite and its Secreted Products

“…Susceptibility to infection with H. polygyrus is controlled to a large degree by the genetic background of the mouse strain ( Table 1); C57BL/6 and CBA mice are highly susceptible 21,22 . For maintenance of the parasite life cycle, the F1 hybrid between these two strains has been chosen for its ability to withstand much higher worm burdens without morbidity (excessive intestinal epithelial damage) compared to either parental strain.…”

The Transcription Factors Thpok and LRF Are Necessary and Partly Redundant for T Helper Cell Differentiation

“…To examine Th2 cell responses, we challenged Thpok-deficient mice with the intestinal helminth Heligmosomoides polygyrus (Behnke et al, 2009), which normally generates a strong IL-4 and IL-13 response by CD4 + Th2 effector cells (Figure 6A). Thpok-deficient mice failed to control the parasite, leading to inflammation, disruption of mucosal architecture, and increased parasite fecundity as assessed by egg counts (Figure 6B).…”

Protein Deficiency and Intestinal Nematode Infection in Pregnant Mice Differentially Impact Fetal Growth through Specific Stress Hormones, Growth Factors, and Cytokines>

“…In a primary infection, stage 4 larvae encyst in the mucosal muscularis for ;1 wk before emerging into the intestinal lumen where they remain as adult worms for several months as a result of their immunosuppressive effect on Th2 immune responses (25). In the H. bakeri trickle infection protocol, which mimics natural environmental conditions, mice are repeatedly exposed to incoming larvae and harbor both larval and adult stages simultaneously, allowing generation of protective Th2 immune responses, including IL-4, IL-5, and IL-13 (26), that delay larval development and increase expulsion of adult worms from the intestine (27).…”