In recent years, evidence is mounting that the crosstalk between the intestinal microbiota and the immune system is modulated by nutrition and that this modulation can have significant impact on intestinal homeostasis and disease. The interplay between nutrients, immunomodulation and the gut microbiome involve a complex network of transcriptional, genetic and epigenetic programs. Increasing our understanding of how these programs are regulated under different dietary conditions (e.g. obesity and malnutrition) and how they are influenced by toxicants associated with nutritional products will help us decipher how this interplay contributes to the pathogenesis of chronic diseases. Nutrition-mediated deregulation of the crosstalk between the immune system and the gut microbiome can lead to both short term and long-term health effects such as a disrupted mucosal barrier; GI-blood bacterial translocation (“leaky gut”) and systemic over-inflammation impacting the gut-brain axis with key alterations in brain physiology and structure. Furthermore, compromised integrative signals between the enteric epithelium, immune, neuronal and glial cells are known to be affected by disease states involving under- and over-nutrition; infection caused by pathogens or pathobionts, and by environmental or microbiota-derived toxins. This can lead to detrimental effects on systemic neuroendocrinological homeostatic regulation, with consequences on physical growth and cognitive development.
In the past decade, great accomplishments have been made in elucidating some of the multifactorial cytokine network and key signaling pathways associated with many GI tract diseases and how these are affected by nutritional states, unbalanced nutrient supply and environmental toxicants. Our improved comprehension of these ill effects with local, inter-organ or systemic consequences may lead to novel insights into the properties of the gut-brain axis. Increasing evidence indicates that a common denominator of many gut-brain related diseases is the elevated inflammatory/oxidative insults that generally arise from the presence of persistent inflammatory and oxidative milieu. The presence of these insults is often associated with the activation of inflammatory immune cells which involves alterations to the intestinal microbiota and is influenced by nutritional compounds. Persistent inflammatory signals and the activation of cell death pathways may lead to disrupted mucosal adaptations and impaired mucosal recovery. However, more intense research is required to create a more comprehensive understanding of the pathophysiological profile of these diseases, particularly in situations in which the disease manifests as a co-morbidity.
This Research Topic aims to document recent advances in the understanding of the mechanisms and pathophysiological processes involved in the complex relationships between nutrition, the immune system and the intestinal microbiota and potential avenues for therapeutic and nutritional intervention. We welcome the submission of Original Research, Review and Mini-Review articles on the following sub-topics:
• Interactions of nutrients, prebiotics/probiotics, environmental toxicants (eg. heavy metals, air pollutants, pesticides etc) with innate and adaptive immune cells involved in cross-talk with the intestinal microbiota.
• Identification and characterization of signaling pathways in immune cells that are modulated by nutritional compounds and influence the cross-talk of immune cells with the gut microbiome.
• The contribution of nutritional genomics, metagenomics, genetic and epigenetic factors during immune-mediated inflammatory processes that lead to mucosal barrier breakdown and deregulation of intestinal homeostatsis.
• Novel nutritional and immunological approaches to reduce excessive inflammation and mucosal damage, by regulating the dysbiotic intestinal microbiota and improving pathways of gut-brain axis.
In recent years, evidence is mounting that the crosstalk between the intestinal microbiota and the immune system is modulated by nutrition and that this modulation can have significant impact on intestinal homeostasis and disease. The interplay between nutrients, immunomodulation and the gut microbiome involve a complex network of transcriptional, genetic and epigenetic programs. Increasing our understanding of how these programs are regulated under different dietary conditions (e.g. obesity and malnutrition) and how they are influenced by toxicants associated with nutritional products will help us decipher how this interplay contributes to the pathogenesis of chronic diseases. Nutrition-mediated deregulation of the crosstalk between the immune system and the gut microbiome can lead to both short term and long-term health effects such as a disrupted mucosal barrier; GI-blood bacterial translocation (“leaky gut”) and systemic over-inflammation impacting the gut-brain axis with key alterations in brain physiology and structure. Furthermore, compromised integrative signals between the enteric epithelium, immune, neuronal and glial cells are known to be affected by disease states involving under- and over-nutrition; infection caused by pathogens or pathobionts, and by environmental or microbiota-derived toxins. This can lead to detrimental effects on systemic neuroendocrinological homeostatic regulation, with consequences on physical growth and cognitive development.
In the past decade, great accomplishments have been made in elucidating some of the multifactorial cytokine network and key signaling pathways associated with many GI tract diseases and how these are affected by nutritional states, unbalanced nutrient supply and environmental toxicants. Our improved comprehension of these ill effects with local, inter-organ or systemic consequences may lead to novel insights into the properties of the gut-brain axis. Increasing evidence indicates that a common denominator of many gut-brain related diseases is the elevated inflammatory/oxidative insults that generally arise from the presence of persistent inflammatory and oxidative milieu. The presence of these insults is often associated with the activation of inflammatory immune cells which involves alterations to the intestinal microbiota and is influenced by nutritional compounds. Persistent inflammatory signals and the activation of cell death pathways may lead to disrupted mucosal adaptations and impaired mucosal recovery. However, more intense research is required to create a more comprehensive understanding of the pathophysiological profile of these diseases, particularly in situations in which the disease manifests as a co-morbidity.
This Research Topic aims to document recent advances in the understanding of the mechanisms and pathophysiological processes involved in the complex relationships between nutrition, the immune system and the intestinal microbiota and potential avenues for therapeutic and nutritional intervention. We welcome the submission of Original Research, Review and Mini-Review articles on the following sub-topics:
• Interactions of nutrients, prebiotics/probiotics, environmental toxicants (eg. heavy metals, air pollutants, pesticides etc) with innate and adaptive immune cells involved in cross-talk with the intestinal microbiota.
• Identification and characterization of signaling pathways in immune cells that are modulated by nutritional compounds and influence the cross-talk of immune cells with the gut microbiome.
• The contribution of nutritional genomics, metagenomics, genetic and epigenetic factors during immune-mediated inflammatory processes that lead to mucosal barrier breakdown and deregulation of intestinal homeostatsis.
• Novel nutritional and immunological approaches to reduce excessive inflammation and mucosal damage, by regulating the dysbiotic intestinal microbiota and improving pathways of gut-brain axis.
