Project description:Group 3 innate lymphoid cells (ILC3s) are abundant in the developing or healthy intestine to critically support tissue homeostasis in response to microbial cues and other environmental signals. However, during gastrointestinal disease including infections, colorectal cancer, or inflammatory bowel disease (IBD), intestinal ILC3 numbers are dramatically reduced and the remaining ILC3s become dysfunctional which fuels disease and barrier breakdown. To define the underlying transcriptomic changes, we employed RNA sequencing of ILC3s from IBD patients. This may help to gain a deeper understanding of the mechanisms driving these alterations and ultimately lead to novel preventive, diagnostic, or therapeutic opportunities in IBD.
Project description:Deficiency in the X-linked inhibitor of apoptosis protein (XIAP) is the cause for the X-linked lymphoproliferative syndrome 2 (XLP2). About one third of all patients suffers from severe and therapy refractory inflammatory bowel disease (IBD), but the exact pathogenesis remains undefined. We examined the differences in gene expression of pediatric XLP2 patients with IBD to healthy controls and pediatric IBD patients.
Project description:Investigation of whole genome gene expression level changes in Inflammatory bowel disease rats after MSC transplantation, compared to IBD control rats, and to explore the mechanism of MSC transplantation. A four chip study using total RNA recovered from two separate IBD rats after MSC transplantation and two separate IBD control rats. Each chip measures the expression level of 26,419 genes from normal rat and IBD rat treated with MSC transplantation.
Project description:16s RNA gene sequencing data from seawater, bed sediment and steel corrosion samples from Shoreham Harbour, UK, collected to allow bacterial species comparisons between microbially influenced corrosion, the surrounding seawater, and the sea bed sediment at the seafloor and 50cm depth below seafloor.
Project description:CD11b+ cells isolated from IBD patient biopsies have distinct transcriptomic signatures based on their location along the GI tract, inflammation status, IBD type, and medication response. These cells also respond to JAK inhibitors by decreasing cytokine output.