About this Research Topic
Intestinal bacteria play a crucial role in maintaining the immune and metabolic homeostasis of the human body. There are many beneficial contributions of intestinal microbiota to human health: maintenance of gut homeostasis, renewal of intestinal epithelial layer, regulation of intestinal barrier integrity, recovery of intestinal epithelial injury, intestinal angiogenesis, maturation of the immune system, production of nutrients (SCFA, amino acids) and vitamins, development of the nervous system and regulation of appetite and behavior. However, this beneficial relationship can also work in reverse because of an altered microbial content, known as dysbiosis.
Today, there is an increasing amount of research that shows that dysbiosis is a major contributory factor of a wide spectrum of diseases from depression to osteoarthritis, many of which result in pain.
The goal of this research topic is to collate evidence pertaining to the gut-brain axis in relation to pain, in the form of clinical evidence or review articles.
We welcome the submission of manuscripts including, but not limited to, the following topics:
• Development of gut microbiota, and beneficial effects on the human body
• Genome and microbiome
• Gut-Brain axis and related disease
- Pain
- Neurodegenerative diseases (Alzheimer’s disease, multiple sclerosis, Parkinson’s disease)
- Psychologic diseases (Autism, anxiety, depression)
• Musculoskeletal system diseases resulting from microbial dysbiosis
- Osteoporosis
- Osteoarthritis
- Rheumatoid arthritis
- Sarcopenia
• Evidence-based medicine for use to improve dysbiosis (probiotics, prebiotics)
Keywords: gut microbiota, gut-brain axis, dysbiosis, musculoskeletal, probiotics, pain
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.