EEN impacts on gut microbiota composition and changes fecal metabolic activity. It is difficult to infer a causative association between such changes and disease improvement, but the results do challenge the current perception of a protective role for F. prausnitzii in CD.

BACKGROUND AND AIMS: It is not clear whether alterations in the intestinal microbiota of children with celiac disease (CD) cause the disease or are a result of disease and/or its treatment with a gluten-free diet (GFD). METHODS: We obtained 167 fecal samples from 141 children (20 with newonset CD, 45 treated with a GFD, 57 healthy children, and 19 unaffected siblings of children with CD) in Glasgow, Scotland. Samples were analyzed by 16S ribosomal RNA sequencing, and diet-related metabolites were measured by gas chromatography. We obtained fecal samples from 13 children with new-onset CD after 6 and 12 months on a GFD. Relationships between microbiota with diet composition, gastrointestinal function, and biomarkers of GFD compliance were explored. RESULTS: Microbiota a diversity did not differ among groups. Microbial dysbiosis was not observed in children with new-onset CD. In contrast, 2.8% (Bray-Curtis

The cytoskeletal protein vimentin plays a key role in positioning of organelles within the cytosol and has been linked to the regulation of numerous cellular processes including autophagy, however, how vimentin regulates autophagy remains relatively unexplored. Here we report that inhibition of vimentin using the steroidal lactone Withaferin A (WFA) causes vimentin to aggregate, and this is associated with the relocalisation of organelles including autophagosomes and lysosomes from the cytosol to a juxtanuclear location. Vimentin inhibition causes autophagosomes to accumulate, and we demonstrate this results from modulation of mechanistic target of rapamycin (mTORC1) activity, and disruption of autophagosome-lysosome fusion. We suggest that vimentin plays a physiological role in autophagosome and lysosome positioning, thus identifying vimentin as a key factor in the regulation of mTORC1 and autophagy.

This study aimed to provide evidence on whether children at risk of gastrointestinal inflammation have increased measurements of faecal calprotectin (FC). Faecal calprotectin was measured in 232 children; 55 children (n=11 treatment naïve) with juvenile idiopathic arthritis (JIA), 63 with coeliac disease (CD); 17 with new diagnosis before and after treatment on gluten free diet and 114 controls. None of the treatment-naive children with JIA had raised FC. Four JIA patients on treatment had a raised FC but in all cases a repeat test was normal. In newly diagnosed CD patients, the median (IQR) FC was higher 36.4 (26-61) than in controls 25.0 (23-41) mg/kg (p=0.045) but this significantly decreased 25 (25-25) mg/kg (p=0.012) after six months on gluten free diet. Random measurements of FC are not raised in children with JIA or CD. A significant elevation of FC in these groups is not explained by their diagnosis and therefore needs further investigation.