The human body is colonized by the microbiota, a complex community of microorganisms, such as bacteria, archaea, fungi, viruses (especially bacteriophages) and protozoans. The gastrointestinal tract exhibits the greatest microbial density and diversity, called gut microbiota (GM), of which microorganisms outnumber the host by more than 25-fold in terms of genetic composition. Unsurprisingly, this vast microbial ecosystem interacts intimately and, for the most part, symbiotically with its human host, performing essential metabolic functions, (i.e polysaccharide fermentation and vitamin biosynthesis) affecting multiple aspects of host physiology, including the immune system development. Microbiota indicates the microbes that collectively inhabit a given ecosystem, whereas microbiome refers to the collection of all genomes of microbes in that ecosystem. Each person’s microbiome is unique, rapidly developing throughout early childhood and with differing rates of variability in adulthood. Variations in microbial composition can be influenced by both genetic and environmental factors, including diet habits, geographical location, toxin/carcinogen exposure, and hormones. GM dysbiosis, meaning imbalances in the composition and function of the intestinal microbes, is associated with the onset of different non-communicable diseases, ranging from cardiovascular, neurologic, respiratory, and metabolic illnesses to cancer.
Chronic inflammation is the common driver of these pathological conditions and it is a well-established effector in atherosclerosis and a marker of increased cardiovascular risk. In addition, it is well recognized that chronic inflammation contributes to about 1 in 4 of all cancer cases. Mediators of the inflammatory response can induce point mutations in tumor suppressor genes, DNA methylation and post-translational modifications, causing alterations in critical pathways responsible for maintaining the normal cellular homeostasis and leading to the development and progression of cancer.
Key questions are:
1) Which are the mechanisms responsible for the interplay among gut microbiota, inflammation and cardiovascular disease?
2) Which are the actions linking gut microbiota, inflammation and cancer?
3) Is the study of these interactions a pathway to improve and “tailor” precision medicine?
4) Does a “healthy diet” exist?
5) Can the intake of functional foods really make any differences?
The aim of this Research Topic is to gather new information regarding the mechanisms regulating the initial phases of these disabling inflammation-based human diseases. In addition, this Research Topic targets at improving the current therapeutic clinical protocols meanwhile reducing the off-target effects.
The human body is colonized by the microbiota, a complex community of microorganisms, such as bacteria, archaea, fungi, viruses (especially bacteriophages) and protozoans. The gastrointestinal tract exhibits the greatest microbial density and diversity, called gut microbiota (GM), of which microorganisms outnumber the host by more than 25-fold in terms of genetic composition. Unsurprisingly, this vast microbial ecosystem interacts intimately and, for the most part, symbiotically with its human host, performing essential metabolic functions, (i.e polysaccharide fermentation and vitamin biosynthesis) affecting multiple aspects of host physiology, including the immune system development. Microbiota indicates the microbes that collectively inhabit a given ecosystem, whereas microbiome refers to the collection of all genomes of microbes in that ecosystem. Each person’s microbiome is unique, rapidly developing throughout early childhood and with differing rates of variability in adulthood. Variations in microbial composition can be influenced by both genetic and environmental factors, including diet habits, geographical location, toxin/carcinogen exposure, and hormones. GM dysbiosis, meaning imbalances in the composition and function of the intestinal microbes, is associated with the onset of different non-communicable diseases, ranging from cardiovascular, neurologic, respiratory, and metabolic illnesses to cancer.
Chronic inflammation is the common driver of these pathological conditions and it is a well-established effector in atherosclerosis and a marker of increased cardiovascular risk. In addition, it is well recognized that chronic inflammation contributes to about 1 in 4 of all cancer cases. Mediators of the inflammatory response can induce point mutations in tumor suppressor genes, DNA methylation and post-translational modifications, causing alterations in critical pathways responsible for maintaining the normal cellular homeostasis and leading to the development and progression of cancer.
Key questions are:
1) Which are the mechanisms responsible for the interplay among gut microbiota, inflammation and cardiovascular disease?
2) Which are the actions linking gut microbiota, inflammation and cancer?
3) Is the study of these interactions a pathway to improve and “tailor” precision medicine?
4) Does a “healthy diet” exist?
5) Can the intake of functional foods really make any differences?
The aim of this Research Topic is to gather new information regarding the mechanisms regulating the initial phases of these disabling inflammation-based human diseases. In addition, this Research Topic targets at improving the current therapeutic clinical protocols meanwhile reducing the off-target effects.
