Abstract
BackgroundThe mammalian intestine is a complex biological system that exhibits functional plasticity in its response to diverse stimuli to maintain homeostasis. To improve our understanding of this plasticity, we performed a high-level data integration of 14 whole-genome transcriptomics datasets from samples of intestinal mouse mucosa. We used the tool Centrality based Pathway Analysis (CePa), along with information from the Reactome database.ResultsThe results show an integrated response of the mouse intestinal mucosa to challenges with agents introduced orally that were expected to perturb homeostasis. We observed that a common set of pathways respond to different stimuli, of which the most reactive was the Regulation of Complement Cascade pathway. Altered expression of the Regulation of Complement Cascade pathway was verified in mouse organoids challenged with different stimuli in vitro.ConclusionsResults of the integrated transcriptomics analysis and data driven experiment suggest an important role of epithelial production of complement and host complement defence factors in the maintenance of homeostasis.
Highlights
The mammalian intestine is a complex biological system that exhibits functional plasticity in its response to diverse stimuli to maintain homeostasis
From the results of the analysis on these datasets we identified the pathway “Regulation of Complement Cascade” that appears to play an important role in the functional plasticity of the intestinal epithelial response to different nutritional, microbial, and chemical challenges
In conclusion, high-level data integration of transcriptomics datasets from intestinal tissue from in vivo experiments was a valuable approach to identify common pathways associated with functional plasticity and intestinal homeostasis
Summary
The mammalian intestine is a complex biological system that exhibits functional plasticity in its response to diverse stimuli to maintain homeostasis. The gut functionalities described above are attributed to groups of genes organised into various functional pathways [21,22,23,24] responding to physiological changes These pathways can be modulated by enteric infection, toxic compounds in food or produced by the microbiota, ionic and osmotic changes as well as substantial variations in nutrient availability. The diverse range of changing conditions encountered at the intestine would require a high-level of functional plasticity compared to other tissues. This theory is supported by the fact that a higher number of genes are expressed in the gut mucosa than that in the heart, liver, kidney, and other organs that
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