Trillions of microbes inhabit the human gut. On the one hand, the host provides the habitat and nutrition for growth and shapes gut microbiota composition and function through dietary habits or ingestion of antibacterial food preservatives and medicinal products. On the other hand, commensal microbes regulate the gut's homeostasis, metabolize nutrients, bile acids, xenobiotics and exert significant modulatory effects on the function of the whole organism. Accumulating evidence suggests that dysbiosis, i.e., the imbalance of the microbiota, is associated with numerous pathological conditions including gastrointestinal diseases, cardiovascular and metabolic diseases, neurological and psychiatric disorders. However, the association between gut dysbiosis and systemic diseases represents a typical example of 'the chicken or the egg' causality dilemma.
The animal brain controls behavior and plays a vital role in regulating cardiovascular, renal, respiratory, gastrointestinal and immunological systems. Recent scientific advances demonstrate a bidirectional interaction between the gut microbiota and brain. First, microbiota-produced metabolites may stimulate sensory fibers of the intrinsic and/or extrinsic nervous system, which communicate with the central nervous system. Secondly, once in the systemic circulation, gut microbes-derived molecules may affect the brain's function either by passing the blood-brain barrier or acting on the circumventricular organs. Finally, neurogenic dysfunction of gastrointestinal control results in dysbiosis.
The collection of articles under this Research Topic aims to explore the cellular and molecular mechanisms by which the gut microbiota impacts brain's function and the brain-controlled functions of the organism. Submissions are welcome for the following article types: original research, review, mini-reviews, research protocol/method, opinion and hypothesis.
Topic editor M. Ufnal is employed by AstraZeneca, a commercial company. All other Topic Editors declare no competing interests with regards to the Research Topic subject.
Trillions of microbes inhabit the human gut. On the one hand, the host provides the habitat and nutrition for growth and shapes gut microbiota composition and function through dietary habits or ingestion of antibacterial food preservatives and medicinal products. On the other hand, commensal microbes regulate the gut's homeostasis, metabolize nutrients, bile acids, xenobiotics and exert significant modulatory effects on the function of the whole organism. Accumulating evidence suggests that dysbiosis, i.e., the imbalance of the microbiota, is associated with numerous pathological conditions including gastrointestinal diseases, cardiovascular and metabolic diseases, neurological and psychiatric disorders. However, the association between gut dysbiosis and systemic diseases represents a typical example of 'the chicken or the egg' causality dilemma.
The animal brain controls behavior and plays a vital role in regulating cardiovascular, renal, respiratory, gastrointestinal and immunological systems. Recent scientific advances demonstrate a bidirectional interaction between the gut microbiota and brain. First, microbiota-produced metabolites may stimulate sensory fibers of the intrinsic and/or extrinsic nervous system, which communicate with the central nervous system. Secondly, once in the systemic circulation, gut microbes-derived molecules may affect the brain's function either by passing the blood-brain barrier or acting on the circumventricular organs. Finally, neurogenic dysfunction of gastrointestinal control results in dysbiosis.
The collection of articles under this Research Topic aims to explore the cellular and molecular mechanisms by which the gut microbiota impacts brain's function and the brain-controlled functions of the organism. Submissions are welcome for the following article types: original research, review, mini-reviews, research protocol/method, opinion and hypothesis.
Topic editor M. Ufnal is employed by AstraZeneca, a commercial company. All other Topic Editors declare no competing interests with regards to the Research Topic subject.
