Role of the Nh (Non-hair) Mutation in the Development of Dermatitis and Hyperproduction of IgE in DS-Nh Mice

Abstract

Abstract:The DS-Nh (DS Non-hair) mouse is a spontaneous hairless mutant of the DS mouse. The inheritance mode of the Nh mutation is autosomal dominant, and the Nh locus is mapped to Chromosome 11. The roles of the Nh mutation in spontaneous dermatitis and IgE hyperproduction were studied using an Nh congenic strain with a genetic background from the BALB/c mouse. In contrast to DS-Nh (Nh/+) mice, BALB/c-Nh (Nh/+) mice under conventional conditions showed a marked increase in serum IgE, without the development of dermatitis. These results suggest that IgE hyperproduction is regulated by the Nh mutation, while other genetic factor(s) are also involved in the development of dermatitis. Key words: dermatitis, DS-Nh mouse, IgE our re-examination using a larger number of animals, however, marked dermatitis with hyperproduction of serum IgE was observed even in the absence of S. aureus under SPF conditions, although the incidence of dermatitis was much lower than in conventional mice [13]. These results suggest that the dermatitis is not triggered by S. aureus infection, but that an IgE antibody-mediated allergic reaction plays a causative role.If that is the case, then genetic analyses of the Nh mutation appear to be necessary to reveal the pathogenesis of the spontaneous dermatitis.This report deals with the inheritance mode of the Nh mutation, chromosomal location of the responsible gene, and the role of the Nh mutation in the spontaneous dermatitis and IgE hyperproduction. An Nh-congenic mouse strain with a genetic background

Effects of zinc deficient diet on development of atopic dermatitis-like eruptions in DS-Nh mice

“…It has been reported that S. aureus on the surface of skin plays an important role in the onset of AD-like lesions in DS-Nh mice and that the number of S. aureus colonies is correlated with symptoms of ADlike lesions [9][10][11], whereas DS-Nh mice maintained in SPF conditions occasionally showed AD-like lesions with increased serum IgE, but no S. aureus growth on the skin surface. These findings suggest that in DS-Nh mice the allergic response including hyperserum IgE was correlated with the onset of ADlike lesions and that S. aureus growth on the skin surface was correlated with exacerbation of symptoms.…”

TRPV3: a ‘more than skinny’ channel

“…The first evidence that TRPV3 is involved in hair growth came from a mouse engineered as a model for Down syndrome crossed with a hair‐less mouse, DS‐Nh . Intriguingly, in breeding studies involving DS‐Nh and Nh mice, positional cloning approaches identified the Gly573Ser mutation of the trpv3 gene as responsible for the spontaneous hairless phenotype in these animals, as well as in hairless WBN/Kob‐Ht rats .…”

WBN/Kob-Ht Rats Spontaneously Develop Dermatitis under Conventional Conditions: Another Possible Model for Atopic Dermatitis

“…We discuss the characteristics of Ht-rats in comparison with Nh-mice, which have recently been proposed as an animal model for human AD [3,4,19].…”

“…The inheritance mode of both mutations is autosomal dominant [1,3]. The Nh locus is mapped on mouse chromosome 11 and the Ht locus on rat chromosome 10 [1,3], and both the genes are located in contiguity with the linkage site (unpublished data). Furthermore, there are some phenotypical similarities between both mutated rodents.…”