Norovirus triggered microbiota-driven mucosal inflammation in interleukin 10-deficient mice.

Background: Infection may trigger clinically overt mucosal inflammation in patients with predisposition for inflammatory bowel disease. However, the impact of particular enteropathogenic microorganisms is ill-defined. In this study, the influence of murine norovirus (MNV) infection on clinical, histopathological, and immunological features of mucosal inflammation in the IL10-deficient (Il10) mouse model of inflammatory bowel disease was examined.

Strain-specific colitis susceptibility in IL10-deficient mice depends on complex gut microbiota-host interactions.

Background: Colitis susceptibility in Il10(-/-) mice depends on genetic background and microbiota composition. A major genetic locus mediating colitis susceptibility, Cdcs1, was transferred from susceptible C3Bir-Il10(-/-) to resistant B6-Il10(-/-) mice, resulting in susceptible congenic BC-R3-Il10(-/-) mice. The aim of this study was to determine the impact of microbiota on this differential colitis susceptibility using a Helicobacter hepaticus infection model.

Analysis of Cd14 as a genetic modifier of experimental inflammatory bowel disease (IBD) in mice.

Background And Aim: By combining QTL and gene expression analyses, we have previously identified Cd14 as a potential candidate gene contributing to the differential IBD susceptibility of C3H/HeJBir (C3/J)-Il10(-/-) mice [carrying IBD-resistance alleles at this QTL (Cdcs6)] and C57BL/6J (B6)-Il10(-/-) mice, corroborating studies that showed an association of a CD14-promoter polymorphism with Crohn's disease and ulcerative colitis. The aim of the present study was to analyze the molecular mechanisms leading to differential intestinal expression of Cd14 and its contribution to IBD development.

Methods: Intestinal CD14 expression was assessed by FACS, immunohistochemistry, and ELISA on supernatants of primary epithelial cell and tissue cultures.

A cathepsin D-cleaved 16 kDa form of prolactin mediates postpartum cardiomyopathy.

Postpartum cardiomyopathy (PPCM) is a disease of unknown etiology and exposes women to high risk of mortality after delivery. Here, we show that female mice with a cardiomyocyte-specific deletion of stat3 develop PPCM. In these mice, cardiac cathepsin D (CD) expression and activity is enhanced and associated with the generation of a cleaved antiangiogenic and proapoptotic 16 kDa form of the nursing hormone prolactin.

[Skin layer thickness at the ear of the domesticated pig , with special reference to the use of the ear integument for human dermatological research].

Based on a shrinkage-free methodical approach (special plastic resin embedding, frozen section technique) and histological routine staining, the thickness of the different skin layers was measured from 15 regions of the outer and the inner side of the porcine auricle. Mean thickness values were for the str. corneum: 19 microns outside/20 microns inside, vital epidermis without ridges: 52 microns outside/56 microns inside, dermis: 1175 microns outside/1112 microns inside, hypodermis: 1024 microns outside/741 microns inside, perichondrium: 295 microns outside/220 microns inside.