Dynamic bidirectional interactions between gut microbiome and the host are critical for gut homeostasis. By the virtue of secretion of mucus, immunological mediators (like IgA and IL22), expression of gut microbial sensors (like toll like receptors [TLRs] and nucleotide-binding and oligomerization domain NOD-like receptors [NLRs]), and microRNAs, intestinal epithelial cells spatially segregate the gut microbiome. Similarly, the gut microbiome as a symbiotic partner, nourishes the colonocytes, participates in establishment of the immune system and provides plethora of metabolites essential for normal gut physiology. This bidirectional interaction is subject to perturbations by various environmental factors, like use of antibiotics and drugs, diet, sex and genetics. Any such perturbation that disrupts the elasticity of the host-microbiome interaction, skews the balance from health to diseased state.
A growing body of evidence, both from human and animal studies implicate altered microbiome composition and/or function in inflammatory diseases of the gastrointestinal (GI) tract. Besides direct damage to the intestinal epithelial lining that restricts the regenerative capacity of the intestine, the dysbiotic microbiome has been shown to disrupt the physiologic exchange (secretion, diffusion, and absorption) across the intestine. This can disturb whole body homeostasis as has been observed in inflammatory GI diseases. Advances in omics technologies (metagenomics, transcriptomics, metabolomics) have yielded significant insights into the role of gut microbiome in GI pathophysiology. This has generally included associations of changes in gut microbial diversity, abundance, or function (changes in levels of metabolites) with clinical features of the disease in humans or preclinical animal models. Due to lack of causal relationships, however, translational and clinical application of these associations is still in infancy.
This Research Topic is expected to yield a better understanding of the interdependence of microbe-metabolite-host interactions in normal physiology and inflammatory disorders of the GI tract. This will permit a mechanistic evaluation of the relationship of gut microbiome with the host opening avenues for the discovery of therapeutic targets for these diseases. We invite colleagues to submit original articles, reviews, mini reviews, perspectives that explore but are not limited to impact of eubiosis and/or dysbiosis in gut mucosal barrier, intestinal epithelial cell function, intestinal epithelial cell metabolism, intestinal immune system, microbial metabolites, colonization resistance in pathogenic insults and inflammatory disorders of the gut.
Dynamic bidirectional interactions between gut microbiome and the host are critical for gut homeostasis. By the virtue of secretion of mucus, immunological mediators (like IgA and IL22), expression of gut microbial sensors (like toll like receptors [TLRs] and nucleotide-binding and oligomerization domain NOD-like receptors [NLRs]), and microRNAs, intestinal epithelial cells spatially segregate the gut microbiome. Similarly, the gut microbiome as a symbiotic partner, nourishes the colonocytes, participates in establishment of the immune system and provides plethora of metabolites essential for normal gut physiology. This bidirectional interaction is subject to perturbations by various environmental factors, like use of antibiotics and drugs, diet, sex and genetics. Any such perturbation that disrupts the elasticity of the host-microbiome interaction, skews the balance from health to diseased state.
A growing body of evidence, both from human and animal studies implicate altered microbiome composition and/or function in inflammatory diseases of the gastrointestinal (GI) tract. Besides direct damage to the intestinal epithelial lining that restricts the regenerative capacity of the intestine, the dysbiotic microbiome has been shown to disrupt the physiologic exchange (secretion, diffusion, and absorption) across the intestine. This can disturb whole body homeostasis as has been observed in inflammatory GI diseases. Advances in omics technologies (metagenomics, transcriptomics, metabolomics) have yielded significant insights into the role of gut microbiome in GI pathophysiology. This has generally included associations of changes in gut microbial diversity, abundance, or function (changes in levels of metabolites) with clinical features of the disease in humans or preclinical animal models. Due to lack of causal relationships, however, translational and clinical application of these associations is still in infancy.
This Research Topic is expected to yield a better understanding of the interdependence of microbe-metabolite-host interactions in normal physiology and inflammatory disorders of the GI tract. This will permit a mechanistic evaluation of the relationship of gut microbiome with the host opening avenues for the discovery of therapeutic targets for these diseases. We invite colleagues to submit original articles, reviews, mini reviews, perspectives that explore but are not limited to impact of eubiosis and/or dysbiosis in gut mucosal barrier, intestinal epithelial cell function, intestinal epithelial cell metabolism, intestinal immune system, microbial metabolites, colonization resistance in pathogenic insults and inflammatory disorders of the gut.
