About this Research Topic
Aging is a main risk for various diseases and pathologies. It associates with immune dysregulation, gut dysbiosis, and a low level of systemic inflammation (referred infammaging). However, the cause of this association remains poorly understood. Although the gut dysbiosis initiates a chain of inflammatory events that culminate in the dysregulation of the innate and adaptive immune system, why does gut dysbiosis occur in healthy aging? Is it always bad?
Why does it change in old mice even when they are kept in the same housing and fed with the same chaw as young mice? Why aging decreases beneficial microbes and accumulates pathogenic commensals in the gut? What does the immune system play in dysbiosis? Is gut dysbiosis reversible, i.e. aging-associated pathologies controllable?
In this new Research Topic, we attempt to answer these questions as overlooked mechanisms to explain manifestation of pathologies in aging, such as cancer, autoimmunity, dementia, and neurodegeneration, including a long prodromal period of Alzheimer’s disease. Despite the chicken and egg conundrum, the Topic is to shed light on importance of crosstalk between microbiome and adaptive immune system as the cause of aging-associated pathologies.
Thus, we aim to recruit cross-disciplinary papers in the fields of immunology, biochemistry, metabolomics, and microbiology, but with primary emphasis on the following topics:
• Dysbiosis in “healthy” aging and its crosstalk with the immune system, which via enrichment of potentially pathogenic immune cells promote diseases in aging.
• The cause of dysbiosis in aging and potential role of adaptive immune cells
• Dysbiosis as a cause of inflammaging that upregulates myelopoiesis and downregulates lymphopoiesis in the bone marrow in aging.
• Commensals, antigen mimicry, and autoimmune response
• Dysbiosis, microbial metabolites, aging pathology.
Why does it change in old mice even when they are kept in the same housing and fed with the same chaw as young mice? Why aging decreases beneficial microbes and accumulates pathogenic commensals in the gut? What does the immune system play in dysbiosis? Is gut dysbiosis reversible, i.e. aging-associated pathologies controllable?
In this new Research Topic, we attempt to answer these questions as overlooked mechanisms to explain manifestation of pathologies in aging, such as cancer, autoimmunity, dementia, and neurodegeneration, including a long prodromal period of Alzheimer’s disease. Despite the chicken and egg conundrum, the Topic is to shed light on importance of crosstalk between microbiome and adaptive immune system as the cause of aging-associated pathologies.
Thus, we aim to recruit cross-disciplinary papers in the fields of immunology, biochemistry, metabolomics, and microbiology, but with primary emphasis on the following topics:
• Dysbiosis in “healthy” aging and its crosstalk with the immune system, which via enrichment of potentially pathogenic immune cells promote diseases in aging.
• The cause of dysbiosis in aging and potential role of adaptive immune cells
• Dysbiosis as a cause of inflammaging that upregulates myelopoiesis and downregulates lymphopoiesis in the bone marrow in aging.
• Commensals, antigen mimicry, and autoimmune response
• Dysbiosis, microbial metabolites, aging pathology.
Keywords: Dysbiosis in healthy aging, Immune senescence, dysregulation, gut microbiome, short chain fatty acis, poly amines, microbila metabolites, neuroinflammation, Alzheimer's disease, Parkinson's disease, cance
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.
