Dietary cellulose induces anti-inflammatory immunity and transcriptional programs via maturation of the intestinal microbiota.
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ABSTRACT:
SUBMITTER: Fischer F
PROVIDER: S-EPMC7583510 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:The timing of lung maturation is controlled precisely by complex genetic and cellular programs. Lung immaturity following preterm birth frequently results in Respiratory Distress Syndrome (RDS) and Broncho-Pulmonary Dysplasia (BPD), which are leading causes of mortality and morbidity in preterm infants. Mechanisms synchronizing gestational length and lung maturation remain to be elucidated. In this study, we designed a genome-wide mRNA expression time-course study from E15.5 to Postnatal Day 0 (PN0) using lung RNAs from C57BL/6J (B6) and A/J mice that differ in gestational length by ?30 hr (B6<A/J). Comprehensive bioinformatics and functional genomics analyses were used to identify key regulators, bioprocesses and transcriptional networks controlling lung maturation. We identified both temporal and strain dependent gene expression patterns during lung maturation. For time dependent changes, cell adhesion, vasculature development, and lipid metabolism/transport were major bioprocesses induced during the saccular stage of lung development at E16.5-E17.5. CEBPA, PPARG, VEGFA, CAV1 and CDH1 were found to be key signaling and transcriptional regulators of these processes. Innate defense/immune responses were induced at later gestational ages (E18.5-20.5), STAT1, AP1, and EGFR being important regulators of these responses. Expression of RNAs associated with the cell cycle and chromatin assembly was repressed during prenatal lung maturation and was regulated by FOXM1, PLK1, chromobox, and high mobility group families of transcription factors. Strain dependent lung mRNA expression differences peaked at E18.5. At this time, mRNAs regulating surfactant and innate immunity were more abundantly expressed in lungs of B6 (short gestation) than in A/J (long gestation) mice, while expression of genes involved in chromatin assembly and histone modification were expressed at lower levels in B6 than in A/J mice. The present study systemically mapped key regulators, bioprocesses, and transcriptional networks controlling lung maturation, providing the basis for new therapeutic strategies to enhance lung function in preterm infants.
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Project description:Iron is an essential metal for both animals and microbiota, and neonates and infants of humans and animals, in general, are at the risk of iron insufficient. However, excess dietary iron usually causes negative impacts on the host and microbiota. This study aimed to investigate over-loaded dietary iron supplementation on growth performance, the distribution pattern of iron in the gut lumen and the host, intestinal microbiota, and intestine gene expression profile of piglets. Sixty healthy weaning piglets were randomly assigned to six groups: fed with diets supplemented with ferrous sulfate monohydrate at the dose of 50ppm (Fe50 group), 100ppm (Fe100 group), 200ppm (Fe200 group), 500ppm (Fe500 group), and 800ppm (Fe800) for three weeks. The results indicated that increasing iron had no effects on growth performance but increased diarrheal risk and iron deposition in intestinal digesta, tissues of intestine and liver, and serum. High iron also reduced serum iron-binding capacity, apolipoprotein, and immunoglobin A. The RNA-sequencing analysis revealed that iron changed colonic gene expression profile, such as interferon gamma-signal transducer and activator of transcription 2 based anti-virus and bacteria gene network. Increasing iron also shifted cecal and colonic microbiota, such as reducing alpha diversity, Clostridiales and Lactobacillus reuteri, and increasing Lactobacillus and Lactobacillus amylovorus. Collectively, this study demonstrated that high dietary iron increased diarrheal incidence, changed intestinal immune response-associated gene expression, and shifts gut microbiota. The results would enhance our knowledge of iron effects on the gut and microbiome in piglets, and further contribute to understanding these aspects in humans.
2020-09-20 | GSE158245 | GEO
Project description:Iron is an essential metal for both animals and microbiota. In general, neonates and infants of humans and animals are at the risk of iron insufficiency. However, excess dietary iron usually causes negative impacts on the host and microbiota. This study aimed to investigate overloaded dietary iron supplementation on growth performance, the distribution pattern of iron in the gut lumen and the host, intestinal microbiota, and intestine transcript profile of piglets. Sixty healthy weaning piglets were randomly assigned to six groups: fed on diets supplemented with ferrous sulfate monohydrate at the dose of 50 ppm (Fe50 group), 100 ppm (Fe100 group), 200 ppm (Fe200 group), 500 ppm (Fe500 group), and 800 ppm (Fe800), separately, for 3 weeks. The results indicated that increasing iron had no significant effects on growth performance, but increased diarrheal risk and iron deposition in intestinal digesta, tissues of intestine and liver, and serum. High iron also reduced serum iron-binding capacity, apolipoprotein, and immunoglobin A. The RNA-sequencing analysis revealed that iron changed colonic transcript profile, such as interferon gamma-signal transducer and activator of transcription two-based anti-infection gene network. Increasing iron also shifted colonic and cecal microbiota, such as reducing alpha diversity and the relative abundance of Clostridiales and Lactobacillus reuteri and increasing the relative abundance of Lactobacillus and Lactobacillus amylovorus. Collectively, this study demonstrated that high dietary iron increased diarrheal incidence, changed intestinal immune response-associated gene expression, and shifted gut microbiota. The results would enhance our knowledge of iron effects on the gut and microbiome in piglets and further contribute to understanding these aspects in humans.
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