Project description:PFAPA, the syndrome of periodic fever associated with aphthous stomatitis, pharyngitis and/or cervical adenitis, is the most common periodic fever disease in children. Cases are mostly sporadic; the etiopathogenesis is unknown. In order to shed more insights into pathogenesis, we performed microarray expression analysis on samples from patients with PFAPA during and between flares, healthy controls and patients with hereditary autoinflammatory diseases during flares. RNA was extracted from whole peripheral blood from six patients with PFAPA syndrome during flares and asymptomatic intervals, six healthy controls and six patients with hereditary autoinflammatory diseases (2 familial Mediterranean fever (FMF), 1 TNF-receptor-asociated periodic fever syndrome (TRAPS) and 3 cryopyrin-associated periodic syndromes (CAPS)).
Project description:This project contains raw data, intermediate files and results is a re-analysis of the publicly available dataset from the PRIDE dataset PXD005780. The RAW files were processed using ThermoRawFileParser, SearchGUI and PeptideShaker through standard settings (see ‘Data Processing Protocol’). This reanalysis work is part of the MetaPUF (MetaProteomics with Unknown Function) project, which is a collaboration between EMBL-EBI and the University of Luxembourg. The dataset was selected with the following conditions: 1. It has been made publicly available in PRIDE and focuses on metaproteomics of the human gut; 2. The corresponding metagenomics assemblies were also available from ENA (European Nucleotide Archive) or MGnify. The processed peptide reports for each sample are available to view at the contig level on the MGnify website. In total, the reanalysis identified 15,417 unique proteins from 15 samples.
Project description:Salmonella enterica serovar Typhi (S. Typhi), a human-restricted pathogen, enters the host through the gut to cause typhoid fever. Recent calculations of the typhoid fever burden estimated that more than 20 million new typhoid fever cases occur in low and middle-income countries, resulting in 129,000-223,000 deaths yearly. Interestingly, upon the resolution of acute disease, 1%-5% of patients become asymptomatic chronic carriers of S. Typhi. Chronically infected hosts are not only critical reservoirs of infection that transmit the disease to naive individuals but are also predisposed to developing gallbladder carcinoma (GBC). Nevertheless, the molecular mechanisms involved in the early interactions between gallbladder epithelial cells and S. Typhi remain largely unknown. Based on our previous studies showing that very closely related S. Typhi strains elicit distinct innate immune responses, we hypothesized that host molecular pathways activated by S. Typhi strains derived from acutely and chronically infected patients will differ. To test this hypothesis, we used a novel human organoid-derived polarized gallbladder monolayer (HODGM) model, and 13 S. Typhi strains derived from acutely (n=6) and chronically (n=7) infected patients. We found that S. Typhi strains derived from acutely and chronically infected patients differentially regulate mitogen-activated protein kinase (MAPK) and S6 transcription factors. This differential regulation impacts, at least in part, the cytokine signaling pathway involved in the production of TNF- and IL-6 and is likely to play a critical role in inducing chronic S. Typhi infection in the gallbladder.