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RNA-seq based transcriptomic profiling of the mouse small intestine response to lipopolysaccharide treatment

ABSTRACT: Purpose:Integrity of the intestinal mucosal barrier is important as a first line of defense against bacteria and endotoxin, we aim to characterize the activation response of intestinal mucosa to LPS exposure in a mouse model. Methods:Intestinal mRNA profiles of LPS challenged and control mice were generated by deep sequencing, in triplicate, using Illumina HiSeq 2000 Results: Using an optimized data analysis pipeline(HISAT2/HT-Seq/DESeq2), 714 differentially expression protein-coding and noncoding genes (cut-off P <0.05) were identified in response to LPS treatment. Conclusions: After LPS chanllenge, hundreds of genes are differentially regulated, and these genes participate in immuse defense, Inflammatory response as well as cell migration and proliferation (GO pathway analysis).

ORGANISM(S): Mus musculus

PROVIDER: GSE97371 | GEO | 2018/04/12

REPOSITORIES: GEO

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Project description:Chorioamnionitis (CA), resulting from intra-amniotic inflammation, is a frequent cause of preterm birth and exposes the immature intestine to bacterial toxins and/or inflammatory mediators before birth via fetal swallowing. This may affect intestinal immune development, interacting with the effects of enteral feeding and gut microbiota colonization just after birth. Using preterm pigs as model for preterm infants, we hypothesized that prenatal exposure to gram-negative endotoxin influences postnatal bacterial colonization and gut immune development. Pig fetuses were given intra-amniotic lipopolysaccharide (LPS) 3 d before preterm delivery by cesarean section, and were compared with litter-mate controls (CON) at birth and after 5 d of formula feeding and spontaneous bacterial colonization. Amniotic fluid was collected for analysis of leukocyte counts and cytokines, and the distal small intestine was analyzed for endotoxin level, morphology and immune cell counts. Intestinal gene expression and microbiota were analyzed by transcriptomics and metagenomics, respectively. At birth, LPS-exposed pigs showed higher intestinal endotoxin, neutrophil/macrophage density and shorter villi. About 1.0% of intestinal genes were affected at birth and DMBT1, a regulator of mucosal immune defense, was identified as the hub gene in the co-expression network. Genes related to innate immune response (TLR2, LBP, CD14, C3, SFTPD), neutrophil chemotaxis (C5AR1, CSF3R, CCL5) and antigen processing (MHC II, CD4) were also affected and expression levels correlated with intestinal neutrophil/macrophage density and amniotic fluid cytokine levels. On day 5, LPS and CON pigs showed similar necrotizing enterocolitis (NEC) lesions, endotoxin levels, morphology, immune cell counts, gene expressions and microbiota (except for difference in some low-abundant species). Our results show that CA markedly affects intestinal genes at preterm birth, including genes related to immune cell infiltration. However, a few days later, following the physiological adaptations to preterm birth, CA had limited effects on intestinal structure, function, gene expression, bacterial colonization and NEC sensitivity. We conclude that short-term, prenatal intra-amniotic inflammation is unlikely to exert marked effects on intestinal immune development in preterm neonates beyond the immediate neonatal period.

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RNA-seq based transcriptomic profiling of the mouse small intestine response to lipopolysaccharide treatment

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