PqqE is a new virulence factor that cleaves junctional adhesion molecule A and disrupts gastric epithelial integrity.

infects approximately half of the world's population and is the strongest risk factor for peptic ulcer disease and gastric cancer, representing a major global health concern. persistently colonizes the gastric epithelium, where it subverts the highly organized structures that maintain epithelial integrity. Here, a unique strategy used by to disrupt the gastric epithelial junctional adhesion molecule-A (JAM-A) is disclosed, using various experimental models that include gastric cell lines, primary human gastric cells, and biopsy specimens of infected and non-infected individuals.

Kidney histologic alterations in α-Galactosidase-deficient mice.

Fabry disease is a rare X-linked disorder caused by mutations in the α-galactosidase gene (GLA), the resultant deficiency of lysosomal α-galactosidase enzyme activity leading to systemic accumulation of globotriaosylceramide and other glycosphingolipids. GLA knockout mice ("Fabry mice") were generated as an animal model for Fabry disease but, as they do not manifest progressive chronic kidney disease (CKD), their relevance as a model for human Fabry nephropathy is uncertain. We evaluated the histological alterations in the kidneys of Fabry mice at different ages, as contrasted to those observed in wild-type mice.

Kidney biopsy findings in heterozygous Fabry disease females with early nephropathy.

Fabry disease is an X-linked glycosphingolipidosis caused by deficiency of alpha-galactosidase. Progressive chronic kidney disease (CKD) is a major cause of morbidity and mortality in males. Although 40% of heterozygous females may develop renal involvement, pathologic data on Fabry nephropathy in heterozygotes are scarce.