Project description:We established a bacteria infective intestinal inflammation in turbot (Scophthalmus maximus). And found that β-glucan could significantly alleviate the phenotype of turbot intestinal inflammation. We performed single cell transcriptome analysis to study bacteria infective intestinal inflammation and the effects of β-glucan. Furthermore, we revealed that β-glucan through activates Th17 cells to alleviate intestinal inflammation in turbot.
Project description:We establish a trained immunity activation model in turbot (Scophthalmus maximus) by training with β-glucan in vivo. Through single cell RNA-sequencing analysis, we annotate 16 clusters of immune cells and blood cells from head kidney and spleen, and successfully characterize that neutrophils exhibit distinguished feature of trained immunity.
Project description:Commensal microbiota contribute to gut homeostasis and influence mucosal gene expression. We harvested mucosal lining of middle and distal part of the small intestine and colon from germ-free (GF) and gnotobiotic mice monocolonized either with the E.coli strain O6K13 (O) or Nissle 1917 strain (N). The expression profiles of the mucosa samples were compared to the corresponding tissue isolated from conventionally reared mice in order to disclose genes differentially expressed in response to the change in the intestinal microflora composition.
Project description:Background: Enteromyxosis caused by the intestinal myxozoan parasite Enteromyxum scophthalmi is a serious threat for turbot (Scophthalmus maximus, L.) aquaculture, causing severe catarrhal enteritis leading to a cachectic syndrome, with no therapeutic options available. There are still many aspects of host-parasite interaction and disease pathogenesis that are yet to be elucidated, and to date, no analysis of the transcriptomic changes induced by E. scophthalmi in turbot organs has been conducted. In this study, RNA-seq technology was applied to head kidney, spleen and pyloric caeca of severely infected turbot with the aim of furthering our understanding of the pathogenetic mechanisms and turbot immune response against enteromyxosis. Results: A huge amount of information was generated with more than 23,000 identified genes in the three organs, amongst which 4,762 were differently expressed (DE) between infected and control fish. Associate gene functions were studied based on gene ontology terms and available literature, and the most interesting DE genes were classified into five categories: 1) immune and defence response; 2) apoptosis and cell proliferation; 3) iron metabolism and erythropoiesis; 4) cytoskeleton and extracellular matrix and 5) metabolism and digestive function. The analysis of down-regulated genes of the first category revealed evidences of a connexion failure between innate and adaptive immune response, especially represented by a high number of DE interferon-related genes in the three organs. Furthermore, we found an intense activation of local immune response at intestinal level that appeared exacerbated, whereas in kidney and spleen genes involved in adaptive immune response were mainly down-regulated. The apoptotic machinery was only clearly activated in pyloric caeca, while kidney and spleen showed a marked depression of genes related to erythropoiesis, probably related to disorders in iron homeostasis. The genetic signature of the causes and consequences of cachexia was also demonstrated by the down-regulation of the genes encoding structural proteins and those involved in the digestive metabolism. Conclusions: This transcriptomic study has enabled us to gain a better understanding of the pathogenesis of enteromyxosis and identify a large number of DE target genes that bring us closer to the development of strategies designed to effectively combat this pathogen. Four samples per organ (kidney, spleen and pyloric caeca) were sequenced by Illumina HiSeq 2000 as 100bp paired-end reads. For each organ, three samples were taken from Enteromyxum severely infected turbot and the remaining one was a pool of three control turbot.