Project description:beta-glucan induced glycolysis in HIF-1 depedent manner. We reported that beta-glucan injection in mice led to upregulated glycolysis. HIF-1a plays a major role in this process. Mice receives beta-glucan via ip for 4 days. Splenocytes were isolated for RNA sequencing.
Project description:We found that beta-glucan treatment induces early induction of transcripts associated with inflammation and metabolism. Several days after beta-glucan treatment, genes associated with differentation and housekeeping remain upregulated. LPS treatment induces a strong inflammatory response. Beta-glucan did not significantly alter the macrophage response to LPS.
Project description:beta-glucan induced glycolysis in HIF-1 depedent manner. We reported that beta-glucan injection in mice led to upregulated glycolysis. HIF-1a plays a major role in this process.
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:Trained immunity, a form of innate immune memory, involves the functional reprogramming of innate immune cells, enabling an enhanced nonspecific response to subsequent challenges. While beta-glucan, a fungal cell wall component, is a known inducer of this process in zebrafish, the specific receptor responsible remains unidentified. Here, we identify C-type lectin domain-containing 1 (CLDC1), designated DrDectin-1, as the pivotal beta-glucan receptor in zebrafish through AI-driven bioinformatic screening based on mammalian Dectin-1. Structural analysis suggests key beta-glucan binding residues (D182, Y183, H184). Using cldc1 knockout zebrafish in beta-glucan training and secondary infection models, combined with RNA-seq, H3K4me3 ChIP-seq, and virtual cell modeling, we demonstrate that CLDC1 mediates trained immunity via the Syk-Raf signaling pathways. Our findings identify the long-sought beta-glucan receptor in zebrafish and provide a comprehensive mechanistic framework for innate immune memory in teleosts, with implications for evolutionary immunology and disease management.
Project description:Trained immunity, a form of innate immune memory, involves the functional reprogramming of innate immune cells, enabling an enhanced nonspecific response to subsequent challenges. While beta-glucan, a fungal cell wall component, is a known inducer of this process in zebrafish, the specific receptor responsible remains unidentified. Here, we identify C-type lectin domain-containing 1 (CLDC1), designated DrDectin-1, as the pivotal beta-glucan receptor in zebrafish through AI-driven bioinformatic screening based on mammalian Dectin-1. Structural analysis suggests key beta-glucan binding residues (D182, Y183, H184). Using cldc1 knockout zebrafish in beta-glucan training and secondary infection models, combined with RNA-seq, H3K4me3 ChIP-seq, and virtual cell modeling, we demonstrate that CLDC1 mediates trained immunity via the Syk-Raf signaling pathways. Our findings identify the long-sought beta-glucan receptor in zebrafish and provide a comprehensive mechanistic framework for innate immune memory in teleosts, with implications for evolutionary immunology and disease management.
Project description:A clone encoding carboxymethylcellulase activity was isolated during functional screening of a human gut metagenomic library using Lactococcus lactis MG1363 as heterologous host. The insert sequence revealed a glycoside hydrolase family 9 (GH9) catalytic domain with sequence similarity to a gene from Coprococcus sp. ART55/1, which is closely related to Coprocococcus eutactus. Surveys of available genomes indicated a limited distribution of GH9 domains among dominant human colonic anaerobes. Genomes of two Coprococcus-related strains showed the presence of two GH9-encoding and four GH5-encoding genes, however, the strains did not appear to be able to degrade cellulose. Instead, they grew well on beta-glucans and one of the strains also showed growth on galactomannan, galactan and glucomannan. Gene expression and proteomic analysis of Coprococcus sp. ART55/1 grown on cellobiose, beta-glucan and lichenan led to a similar change in expression in comparison to glucose. On beta-glucan and lichenan only, one of the four GH5 genes was strongly upregulated. Growth on glucomannan lead to a transcriptional response of many genes, in particular a strong upregulation of glycoside hydrolases involved in mannan degradation. Thus, beta-glucans are a major growth substrate for species related to Coprococcus eutactus, with glucomannan and galactans alternative substrates for some strains.
