Project description:To investigate the effect of short distance transport on jejunal tissueof weaned piglets, We then performed gene expression profiling analysis using data obtained from RNA-seq in jejunal tissues of weaned piglets after transport and without transport
Project description:The study investigated the impact of environment on the composition of the gut microbiota and mucosal immune development and function at gut surfaces in early and adult life. Piglets of similar genotype were reared in indoor and outdoor environments and in an experimental isolator facility. Mucosa-adherent microbial diversity in the pig ileum was characterized by sequence analysis of 16S rRNA gene libraries. Host-specific gene responses in gut ileal tissues to differences in microbial composition were investigated using Affymetrix microarray technology and Real-time PCR. Experiment Overall Design: Animals were reared on the sow at an outdoor or indoor facility. Additional piglets from the indoor facility were transferred to individual isolator units at 24 hours of age, and given a daily dose of antibiotic cocktail for the duration of the study. Piglets were weaned at day 28. From day 29 onwards, piglets were fed creep feed ad libitum. Ileal tissue samples were excised from N=6 piglets per group at day 5, 28 and 56.
Project description:Transcriptional profiling of 25d old piglets comparing control untreated suckling jejunum with weaned piglets' jejunum. The goal was to gain new insight into the interaction between weaning and intestinal function.A keen interest is paid in deciphering expression changes of apoptosis or cell cycle control genes. The statistical analysis of gene ontology revealed that most of these altered genes are metabolic-related enzymes and regulators which may involved in the biological regulation, developmental process, and cellular process. Weaning also causes alterations in various immune response pathways. Results likely indicate that weaning induced cell cycle arrest, enhanced apoptosis, and inhibited cell proliferation. Two-condition experiment, suckling control piglets' jejunum vs. weaned piglets' jejunum. Biological replicates: 4 control replicates, 4 weaned replicates.
Project description:The transcriptome changes of the ileal mucosa in suckling piglets during early postnatal life were analysed to contribute to the knowledge of a pig’s gut development. In addition, the ileal transcriptome of suckling piglets was compared with that of age-matched weaned piglets (weaned at the age of 21 days) to elucidate the effect of weaning on the developing gut. DNA microarray was used to analyse the change of transcriptome profiles and biological pathways in porcine ileum that occurred during the developmental or the weaning process.
Project description:In order to test the development of gastrointestinal tract (GIT) in pre-weaned cavles, the GIT tissues were collected from day 0, day 7, day 21 and day 42 calves. RNA-seq was used to measure the transcriptome profiles. The RNA-seq analysis revealed the fast development of small intestine and rumen tissue during the first week after birth.
Project description:Neural control of visceral organ function is essential for homeostasis and health. Intestinal peristalsis is critical for digestive physiology and host defence and is often dysregulated in gastrointestinal (GI) disorders. Luminal factors, such as diet and microbiota regulate neurogenic programs of gut motility, but the underlying molecular mechanisms remain unclear. Here we show that the transcription factor Aryl hydrocarbon Receptor (AhR) functions as a biosensor in intestinal neural circuits linking their functional output to the microbial environment of the gut lumen. Using nuclear RNA sequencing of mouse enteric neurons representing distinct intestinal segments and microbiota states, we demonstrate that the intrinsic neural networks of the colon exhibit unique transcriptional profiles controlled by the combined effects of host genetic programmes and microbial colonisation. Microbiota-induced expression of AhR in neurons of the distal gastrointestinal tract enables them to respond to the luminal environment and induce expression of neuron-specific effector mechanisms. Neuron-specific deletion of Ahr or constitutive overexpression of its negative feedback regulator CYP1A1, results in reduced peristaltic activity of the colon, similar to that observed in microbiota-depleted mice. Finally, expression of Ahr in enteric neurons of antibiotic-treated mice partially restores intestinal motility. Taken together, our experiments identify AhR signalling in enteric neurons as a regulatory node that integrates the luminal environment with the physiological output of intestinal neural circuits towards gut homeostasis and health. The enteric nervous system (ENS) encompasses the intrinsic neural networks of the gastrointestinal (GI) tract, which regulate most aspects of intestinal physiology, including peristalsis. In addition to host-specific genetic programmes, microbiota and diet have emerged as critical regulators of gut tissue physiology and changes in the microbial composition of the lumen often accompany GI disorders. However the molecular mechanisms by which gut enviromental factors regulate ENS homeostasis remain unknown. In order to address this issue, we used RNA sequencing to identify genes specifically upregulated in mouse colonic neurons in response to microbial colonisation.
Project description:Neural control of visceral organ function is essential for homeostasis and health. Intestinal peristalsis is critical for digestive physiology and host defence and is often dysregulated in gastrointestinal (GI) disorders. Luminal factors, such as diet and microbiota regulate neurogenic programs of gut motility, but the underlying molecular mechanisms remain unclear. Here we show that the transcription factor Aryl hydrocarbon Receptor (AhR) functions as a biosensor in intestinal neural circuits linking their functional output to the microbial environment of the gut lumen. Using nuclear RNA sequencing of mouse enteric neurons representing distinct intestinal segments and microbiota states, we demonstrate that the intrinsic neural networks of the colon exhibit unique transcriptional profiles controlled by the combined effects of host genetic programmes and microbial colonisation. Microbiota-induced expression of AhR in neurons of the distal gastrointestinal tract enables them to respond to the luminal environment and induce expression of neuron-specific effector mechanisms. Neuron-specific deletion of Ahr or constitutive overexpression of its negative feedback regulator CYP1A1, results in reduced peristaltic activity of the colon, similar to that observed in microbiota-depleted mice. Finally, expression of Ahr in enteric neurons of antibiotic-treated mice partially restores intestinal motility. Taken together, our experiments identify AhR signalling in enteric neurons as a regulatory node that integrates the luminal environment with the physiological output of intestinal neural circuits towards gut homeostasis and health. The enteric nervous system (ENS) encompasses the intrinsic neural networks of the gastrointestinal (GI) tract, which regulate most aspects of intestinal physiology, including peristalsis. In addition to host-specific genetic programmes, microbiota and diet have emerged as critical regulators of gut tissue physiology and changes in the microbial composition of the lumen often accompany GI disorders. We found that gut environmental sensor Aryl hydrocarbon receptor (AhR) is induced in colonic neurons in response to microbiota colonisation and regulates intestinal peristalsis in an AhR ligand-dependent manner. In this experiment, we used RNA sequencing to identify genes regulated in mouse colonic neurons by AhR activation.
Project description:Neural control of visceral organ function is essential for homeostasis and health. Intestinal peristalsis is critical for digestive physiology and host defence and is often dysregulated in gastrointestinal (GI) disorders. Luminal factors, such as diet and microbiota regulate neurogenic programs of gut motility, but the underlying molecular mechanisms remain unclear. Here we show that the transcription factor Aryl hydrocarbon Receptor (AhR) functions as a biosensor in intestinal neural circuits linking their functional output to the microbial environment of the gut lumen. Using nuclear RNA sequencing of mouse enteric neurons representing distinct intestinal segments and microbiota states, we demonstrate that the intrinsic neural networks of the colon exhibit unique transcriptional profiles controlled by the combined effects of host genetic programmes and microbial colonisation. Microbiota-induced expression of AhR in neurons of the distal gastrointestinal tract enables them to respond to the luminal environment and induce expression of neuron-specific effector mechanisms. Neuron-specific deletion of Ahr or constitutive overexpression of its negative feedback regulator CYP1A1, results in reduced peristaltic activity of the colon, similar to that observed in microbiota-depleted mice. Finally, expression of Ahr in enteric neurons of antibiotic-treated mice partially restores intestinal motility. Taken together, our experiments identify AhR signalling in enteric neurons as a regulatory node that integrates the luminal environment with the physiological output of intestinal neural circuits towards gut homeostasis and health. The enteric nervous system (ENS) encompasses the intrinsic neural networks of the gastrointestinal (GI) tract, which regulate most aspects of intestinal physiology, including peristalsis. In addition to host-specific genetic programmes, microbiota and diet have emerged as critical regulators of gut tissue physiology and changes in the microbial composition of the lumen often accompany GI disorders. However the molecular mechanisms by which gut enviromental factors regulate ENS homeostasis remain unknown. In order to address this issue, we used RNA sequencing to identify genes specifically upregulated in mouse colonic neurons in response to microbial colonisation.
Project description:Microbiome analysis has relied largely on metagenomics to characterize microbial populations and predict their functions. Here, we used a TMT LC-MSMS metaproteomic analysis of the fecal microbiome in piglets before and after weaning to compare protein abundances as they pertain to microbial populations specific to either a milk- or plant-based diet. Fecal samples were collected from six piglets on the day of weaning and four weeks after transitioning to a standard nursery diet. Using the 12,554 protein groups identified in samples, we confirmed the shift in protein composition that takes place in response to the microbial succession following weaning and demonstrated the redundancy in metabolic processes between taxa. We identified taxa with roles as primary degraders based on corresponding proteins synthesized, thereby providing evidence for cross-feeding. Proteins associated with the breakdown of milk-specific carbohydrates were common among pre-weaned pigs, whereas the proteome of post-weaned piglets contained a greater abundance of proteins involved in the breaking down plant-specific carbohydrates. Furthermore, output revealed that production of propionate takes place via the propionaldehyde pathway in pre-weaned piglets, but changes to production via the succinate pathway in post-weaned piglets. Finally, a disproportionate quantity of carbohydrate-active enzymes (CAZymes) (~8%) were produced by fungi, which typically only represent ~0.1% of the microbiome taxa. Information gathered through this characterization of the metaproteome before and after weaning revealed important differences regarding the role of members in the microbial community, thereby providing information for the optimization of diets and products for both piglet and microbiome health.