As RBP-J was not deleted in the lung, these data show that the skin barrier defect served as a primary risk factor for development of asthma in the normal lung (Demehri et al., 2008).
mdr1a−/− mice infected with Helicobacter spp. may provide a useful tool to explore the pathogenesis of microbial-induced IBD in a model with a presumed epithelial cell "barrier" defect.
These neuronal effects are particularly intriguing given our current understanding of the immunopathogenesis of Crohn's disease, in which intestinal barrier defect is suspected to at least partly drive the immune hyper-reactivity and ensuing inflammation.
Furthermore, no abnormal biological response (i.e., inflammation, vascularization, and the barrier defect of epithelia) or no optical functional change on optically cleared dermis was observed during its 4-week autogenic transplantation into rabbit corneal stromal pocket.
The horizontal and vertical distances between trees and high-voltage transmission lines affect the safe operation of the transmission lines, and different distances between trees and different voltage levels of the transmission lines lead to different levels of tree barrier defect.
Together these points support the microbial contribution to IBD, indicating that a basic antimicrobial mucosal barrier defect could be responsible for susceptibility to this disease.
The acs-22 mutants rarely showed a barrier defect, whereas acs-20 acs-22 acs-20 acs-22 acs-20 acs-22 doubleted barrier function.
acs-22 mutants rarely exhibited a barrier defect, but the acs-20 acs-22 acs-20 acs-22 acs-20 acs-22ly doubleted barrier function, suggesting a redundant function of the genes.
We propose two possible causes of the cuticle barrier defect: Given that acs-20 mutants displayed an unusual accumulation of collagen-like matrix under the alae, one possibility is an alteration of the secretion process of ECM from epithelial cells that results in the barrier defect.
Transgene expression could be suppressed by supplementation with Dox as expected and mice maintained on Dox during embryonic development and in the post-natal period were normal at birth, did not have an epidermal barrier defect and survived to adulthood.
The marked barrier defect in gluten-sensitized mice treated with indomethacin may not only allow an increased influx of gliadin peptides across the epithelium but also of other luminal antigens such as intestinal microbiota with potential bystander, pro-inflammatory effects.
