About this Research Topic
There are two types of stress, distress and eustress. An Enriched Environment (EE) has been demonstrated to induce eustress in residents. EE-induced eustress is not only beneficial to our mental health though affecting brain function, but also enhances our body's defense mechanism. This has been shown for both acquired immunity and innate immunity, against microorganisms, viruses and cancer. EE activates Natural Killer (NK) cells and alters macrophage functions. Activated NK cells can kill pathogens and cancer cells directly, or can promote an anti-cancer microenvironment modulating the innate and adaptive immune response. Macrophages with altered functions, on the other hand, would affect the inflammatory response and acquired immunity. The effects of EE are sometimes mediated through Brain-Derived Neurotrophic Factor (BDNF) production and sympathetic nerve activation.
EE augments our body’s defense mechanisms, thereby preventing carcinogenesis, cancer development and inflammatory diseases or removing pathogens. Among innate immune cells, NK cells are able to kill cancer cells. Further, M2 macrophages play a role in the resolution of inflammation and tissue repair, whereas M1 macrophages cause inflammation, leading to neutrophil infiltration and bacterial killing. Therefore, we would like to tackle the effect of EE on these two types of cells and the underlying mechanism in this Research Topic. Transcriptome analysis, single cell analysis and imaging technique would provide novel insights into these problems.
We welcome Original Research or Review articles focusing on, but not limited to, the following subtopics:
• The underlying mechanism for EE-induced NK cell activation and infiltration
• The underlying mechanism for EE-induced alteration of macrophage function
• The mechanism underlying the different mode of alteration of macrophage function in terms of M1 and M2 dichotomy and tissues
• Changes of inflammatory responses or acquired immunity by altered macrophages
• Effects of environmental stimuli on the anticancer activity of innate immune cells
• NK cells-nervous system interaction in health and diseases
• Identification of cell types responsible for EE-induced BDNF production
• The effect of activated sympathetic nerves on NK cells and macrophages
EE augments our body’s defense mechanisms, thereby preventing carcinogenesis, cancer development and inflammatory diseases or removing pathogens. Among innate immune cells, NK cells are able to kill cancer cells. Further, M2 macrophages play a role in the resolution of inflammation and tissue repair, whereas M1 macrophages cause inflammation, leading to neutrophil infiltration and bacterial killing. Therefore, we would like to tackle the effect of EE on these two types of cells and the underlying mechanism in this Research Topic. Transcriptome analysis, single cell analysis and imaging technique would provide novel insights into these problems.
We welcome Original Research or Review articles focusing on, but not limited to, the following subtopics:
• The underlying mechanism for EE-induced NK cell activation and infiltration
• The underlying mechanism for EE-induced alteration of macrophage function
• The mechanism underlying the different mode of alteration of macrophage function in terms of M1 and M2 dichotomy and tissues
• Changes of inflammatory responses or acquired immunity by altered macrophages
• Effects of environmental stimuli on the anticancer activity of innate immune cells
• NK cells-nervous system interaction in health and diseases
• Identification of cell types responsible for EE-induced BDNF production
• The effect of activated sympathetic nerves on NK cells and macrophages
Keywords: enriched environment, NK cells, macrophages, sympathetic nerves, brain, cancer, inflammation
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.
