Project description:Studying the effect of Th2 cytokine IL13 on on gene expression of human neutrophils by comparing gene expression of neutrophiles isolated from the blood of 3 healthy donors and stimulated with IL-13 (10ng/ml) or left unstimulated.
Project description:Studying the effect of Th2 cytokine IL4 on gene expression of human neutrophils by comparing gene expression of neutrophils isolated from the blood of 3 healthy donors and stimulated with IL-4 (1ng/ml) or left unstimulated.
Project description:Interleukin (IL)-4 and IL-13 are related cytokines with well-known roles in type 2 immune response. However, their effects on neutrophils are less defined and existing research has provided somewhat contradictory results We measured IL-4-, IL-13- and IFN-g-stimulated gene expression in highly purified human neutrophils.
Project description:3 eosinophilic esophagitis biopsies, cultured and stimulated with IL-13 : each of them was either left unstimulated or stimulated (100ng for 48h); We used microarray to uncover the IL-13-induced genes in esophageal epithelial cells of the esophagus Experiment Overall Design: 3 biopsies from EE patients were obtained and primary epithelial cell were cultured and either left unstimulated or stimulated with IL-13 followed by RNA extraction and hybridization on Affymetrix microarrays.
Project description:Allergic asthma is a chronic inflammatory airway disease driven by the cytokine interleukin-13 (IL-13). Although IL-13 signals through the canonical JAK1/TYK2/STAT6 pathway, our understanding of the totality of IL-13-induced signaling intermediates is incomplete. To address this, we performed an unbiased phospho-proteomic analysis of IL-13-stimulated A549 human airway epithelial cells. IL-13 stimulation led to differential phosphorylation at 145 unique serine/threonine residues across 97 proteins involved in diverse cellular processes. These processes included RNA splicing, cytoskeletal remodeling, GTPase activity, and focal adhesion complex formation. Network analysis identified SRC, a non-receptor tyrosine kinase, as a potential upstream regulator of IL-13-induced changes in phosphorylation. Kinetic molecular approaches confirmed that SRC is rapidly activated following IL-13 stimulation, prior to activation of the canonical IL-13 signaling intermediate STAT6 in both human and mouse lung fibroblasts. Pharmacological inhibition of SRC reduced IL-13–induced STAT6 phosphorylation and downstream gene expression in vitro. In vivo, SRC antagonism attenuated IL-13–induced airway hyperresponsiveness (AHR) without significantly affecting inflammatory cell infiltration or gene expression in bronchoalveolar lavage fluid. These findings identify SRC as a novel and selective mediator of IL-13–driven airway responses and suggest that targeting SRC may offer therapeutic benefit in allergic asthma.
Project description:This experiment aims to identify the biological pathways and diseases associated with the cytokine Interleukin 13 (IL-13) using gene expression measured in peripheral blood mononuclear cells (PBMCs). The experiment comprised of samples obtained from 3 healthy donors. The expression profiles of in vitro IL-13 stimulation were generated using RNA-seq technology for 3 PBMC samples at 24 hours. The transcriptional profiles of PBMCs without IL-13 stimulation were also generated to be used as controls. An IL-13R-alpha antagonist (Redpath et al. Biochemical Journal, 2013) was introduced into IL-13 stimulated PBMCs and the gene expression levels after 24h were profiled to examine the neutralization of IL-13 signaling by the antagonist.