-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
-
Cosmetic Ingredient
- Water Treatment Chemical
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
Written and compiledHu Xiaohua's "Collector's Edition" Science Thematic Review of Inflammation (1)Review of the Past and Knowledge of Inflammation Biology "Collector's Edition" Science Inflammation Thematic Review (2)The Genetic Mechanism of Virus Infection Brain and Stomach The gut is an important sensory organ responsible for detecting, transmitting, integrating and responding to various signals from inside and outside the body, and between them forms a two-way information exchange system called the gut-brain ax.
The dysfunction of the gut-brain axis is related to the occurrence of various diseas.
Recent studies have shown that the gut-brain axis can regulate the immune homeostasis of the body by mediating inflammatory signal transduction, thus playing an important role in a variety of inflammatory diseas.
Recently, Gulistan Agirman et .
from the Department of Integrative Biology and Physiology at UCLA published a review in Science entitled Signaling inflammation across the gut-brain axis, exploring the molecules of inflammatory signaling based on the gut-brain ax.
and cellular mechanisms, and the role of the gut-brain axis in inflammatory diseas.
Cells involved in inflammatory signaling in the gut-brain axis are in direct contact with food- and environmental-derived antigens, gut microbes, and their metabolites, so in addition to physical barriers such as the gut-vascular barrier (GVB), the gut is also The human body has the highest number of immune cel.
In the gut, the innate and adaptive immune systems work together to rapidly respond to intestinal damage (see Table 1 for specific immune cell type.
In addition to immune cells, neurons and glial cells in the enteric nervous system are also involved in intestinal immunity, and their dysfunction can alter normal gut-brain communication and central nervous system (CNS) control of the g.
Under normal physiological conditions, the CNS is separated from the peripheral environment by the blood-brain barrier (BB.
In addition, the CNS also contains a certain number of immune cells, such as microglia, astrocytes, and NK cells (see Table
Although meningeal monocytes, neutrophils, and some B cell subsets are directly supplied by the cranial and spinal bone marrow, these CNS-related immune cells are mainly derived from the periphery of the C.
A complex network of interactions is formed between these immune and non-immune cells to regulate inflammatory responses in the central nervous system and gastrointestinal tra.
Table 1 Immune cells involved in inflammatory signaling in the gut-brain axis Mode of inflammatory signaling in the gut-brain axis The transmission of inflammatory signaling in the gut-brain axis is bidirectional, and they can transmit inflammation through three parallel but interconnected pathways Signals: System-humoral pathwa.
Intestinal inflammation caused by local infection, dysbacteriosis or food antigens will release pro-inflammatory cytokines such as IFN-γ, IL-1β, IL-6, TNF-α into the circulatory syst.
These cytokines disrupt the integrity of the GVB and BBB, thereby providing a pathway for intestinal-derived small molecules, toxins, and pathogens to enter the brain parenchyma, ultimately activating CNS immune cells and triggering neuroinflammati.
For example, short-chain fatty acids (SCFAs) produced by gut microbiota can modulate host neuroinflammation by regulating BBB permeability and microglial functi.
The hypothalamic-pituitary-adrenal axis (HPA axis) is an important way for the brain to transmit signals to the gut through the humoral pathway: the peripheral response to environmental stress or intestinal inflammation will trigger the HPA axis through the CNS to coordinate the production of adrenal glucocorticoi.
Released, this stress hormone restores homeostasis and promotes repair of gastrointestinal function by modulating gut immune cell activity, gut function, and microbial compositi.
In addition, the meningeal lymphatic vessels responsible for draining cerebrospinal fluid may be another pathway for signaling molecules to enter the periphery from the CNS to stimulate immune responses in the gastrointestinal tract, but the role of this pathway in gut-brain communication still requires more experimental evidence to suppo.
cellular immune pathwa.
In addition to the endocrine signaling of immune factors across the gut-brain axis, gut immune cells themselves can also directly regulate neuroimmune homeostasis and inflammatory responses in the bra.
Gut antigens stimulate B cell differentiation into IgA+ plasma cells to control gut microbiota homeostasis, and in neurological autoimmune diseases, IgA+ plasma cells are recruited to the brain and spinal cord to reduce neuroinflammati.
In addition, immune cells in the CNS may also be regulated by gut-derived immune cel.
In general, although there are multiple examples of immune cells entering the brain from the gut, studies of immune cells from the brain to the gut are ra.
neural pathwa.
Nerve cells are the "bridge" connecting the CNS and the gastrointestinal tract, and stimulate the CNS inflammatory response to restore homeostasis by transmitting inflammatory signals, such as the vagal nerve (vagal neuron) and dorsal root ganglia (DR.
Taking DRG as an example, in addition to promoting inflammatory pain, DRG nociceptor neurons have been shown to be protective against intestinal pathogenic infectio.
However, whether these effects require negative feedback regulation of the central nervous system is unclear, so more research is necessary to reveal the modulation of the spinal cord efferent pathways in the g.
Gut-brain axis and inflammatory diseases A variety of neurological diseases have been found to coexist with intestinal inflammation, such as autism spectrum disorder (ASD) and age-related cognitive decli.
In a mouse model of ASD, maternal infection or immune activation during pregnancy induces DCs in the gut to differentiate into TH17 cells, and IL-17 produced by TH17 cells crosses the placental barrier and affects the developing CNS, resulting in the appearance of offspri.
Autism phenoty.
In a diet-induced mouse obesity model, a high-fat diet induces the release of cytokines such as IL-1β, IL-6, and TNF-α from microglia, causing inflammation in the middle hypothalamus, resulting in an anxiety-like phenoty.
In addition, migration of intestinal immune cells to the CNS is associated with the pathogenesis of several neurodegenerative diseases, such as multiple sclerosis (MS), Parkinson's disease (PD) and stro.
In addition, the growing understanding of the gut-brain axis has also led to the development of treatments for intestinal diseases, such as inflammatory bowel disease (IBD) and irritable bowel syndrome (IB.
Summary and prospect The bidirectional communication of inflammatory signals based on the gut-brain axis is very important for regulating some normal physiological behaviors and the pathology of inflammation-related diseases, but there are still many important mechanistic questions that remain unanswered: from the afferent direction (from the Intestine to brain), intestinal immune cells can be directly recruited to the brain, but how the brain senses the initial inflammatory signal and its specific mechanism of action is unclear; while in the efferent direction (from brain to intestine), How the brain regulates intestinal inflammation is poorly understo.
The gut microbiota has now emerged as a key regulator of immune cells in the gut-brain axis, and dysbiosis has been shown to be associated with risk factors for multiple inflammatory diseases, but whether dysbiosis is responsible for this chain of events remains to be se.
unanswered questio.
Therefore, deciphering inflammatory signaling mechanisms based on the gut-brain axis is not only critical for our understanding of neural and immune communication, but also for advances in immunotherapy for gastrointestinal and neurological diseas.
Link to the original text: http://d.
org/11126/scien.
abi6087 Publisher: 11 Reprint Notice [Non-original article] The copyright of this article belongs to the author of the article, and personal sharing is welco.
Reprinting is prohibited without permissi.
The author owns all legal rights, and violators will be prosecut.
The dysfunction of the gut-brain axis is related to the occurrence of various diseas.
Recent studies have shown that the gut-brain axis can regulate the immune homeostasis of the body by mediating inflammatory signal transduction, thus playing an important role in a variety of inflammatory diseas.
Recently, Gulistan Agirman et .
from the Department of Integrative Biology and Physiology at UCLA published a review in Science entitled Signaling inflammation across the gut-brain axis, exploring the molecules of inflammatory signaling based on the gut-brain ax.
and cellular mechanisms, and the role of the gut-brain axis in inflammatory diseas.
Cells involved in inflammatory signaling in the gut-brain axis are in direct contact with food- and environmental-derived antigens, gut microbes, and their metabolites, so in addition to physical barriers such as the gut-vascular barrier (GVB), the gut is also The human body has the highest number of immune cel.
In the gut, the innate and adaptive immune systems work together to rapidly respond to intestinal damage (see Table 1 for specific immune cell type.
In addition to immune cells, neurons and glial cells in the enteric nervous system are also involved in intestinal immunity, and their dysfunction can alter normal gut-brain communication and central nervous system (CNS) control of the g.
Under normal physiological conditions, the CNS is separated from the peripheral environment by the blood-brain barrier (BB.
In addition, the CNS also contains a certain number of immune cells, such as microglia, astrocytes, and NK cells (see Table
Although meningeal monocytes, neutrophils, and some B cell subsets are directly supplied by the cranial and spinal bone marrow, these CNS-related immune cells are mainly derived from the periphery of the C.
A complex network of interactions is formed between these immune and non-immune cells to regulate inflammatory responses in the central nervous system and gastrointestinal tra.
Table 1 Immune cells involved in inflammatory signaling in the gut-brain axis Mode of inflammatory signaling in the gut-brain axis The transmission of inflammatory signaling in the gut-brain axis is bidirectional, and they can transmit inflammation through three parallel but interconnected pathways Signals: System-humoral pathwa.
Intestinal inflammation caused by local infection, dysbacteriosis or food antigens will release pro-inflammatory cytokines such as IFN-γ, IL-1β, IL-6, TNF-α into the circulatory syst.
These cytokines disrupt the integrity of the GVB and BBB, thereby providing a pathway for intestinal-derived small molecules, toxins, and pathogens to enter the brain parenchyma, ultimately activating CNS immune cells and triggering neuroinflammati.
For example, short-chain fatty acids (SCFAs) produced by gut microbiota can modulate host neuroinflammation by regulating BBB permeability and microglial functi.
The hypothalamic-pituitary-adrenal axis (HPA axis) is an important way for the brain to transmit signals to the gut through the humoral pathway: the peripheral response to environmental stress or intestinal inflammation will trigger the HPA axis through the CNS to coordinate the production of adrenal glucocorticoi.
Released, this stress hormone restores homeostasis and promotes repair of gastrointestinal function by modulating gut immune cell activity, gut function, and microbial compositi.
In addition, the meningeal lymphatic vessels responsible for draining cerebrospinal fluid may be another pathway for signaling molecules to enter the periphery from the CNS to stimulate immune responses in the gastrointestinal tract, but the role of this pathway in gut-brain communication still requires more experimental evidence to suppo.
cellular immune pathwa.
In addition to the endocrine signaling of immune factors across the gut-brain axis, gut immune cells themselves can also directly regulate neuroimmune homeostasis and inflammatory responses in the bra.
Gut antigens stimulate B cell differentiation into IgA+ plasma cells to control gut microbiota homeostasis, and in neurological autoimmune diseases, IgA+ plasma cells are recruited to the brain and spinal cord to reduce neuroinflammati.
In addition, immune cells in the CNS may also be regulated by gut-derived immune cel.
In general, although there are multiple examples of immune cells entering the brain from the gut, studies of immune cells from the brain to the gut are ra.
neural pathwa.
Nerve cells are the "bridge" connecting the CNS and the gastrointestinal tract, and stimulate the CNS inflammatory response to restore homeostasis by transmitting inflammatory signals, such as the vagal nerve (vagal neuron) and dorsal root ganglia (DR.
Taking DRG as an example, in addition to promoting inflammatory pain, DRG nociceptor neurons have been shown to be protective against intestinal pathogenic infectio.
However, whether these effects require negative feedback regulation of the central nervous system is unclear, so more research is necessary to reveal the modulation of the spinal cord efferent pathways in the g.
Gut-brain axis and inflammatory diseases A variety of neurological diseases have been found to coexist with intestinal inflammation, such as autism spectrum disorder (ASD) and age-related cognitive decli.
In a mouse model of ASD, maternal infection or immune activation during pregnancy induces DCs in the gut to differentiate into TH17 cells, and IL-17 produced by TH17 cells crosses the placental barrier and affects the developing CNS, resulting in the appearance of offspri.
Autism phenoty.
In a diet-induced mouse obesity model, a high-fat diet induces the release of cytokines such as IL-1β, IL-6, and TNF-α from microglia, causing inflammation in the middle hypothalamus, resulting in an anxiety-like phenoty.
In addition, migration of intestinal immune cells to the CNS is associated with the pathogenesis of several neurodegenerative diseases, such as multiple sclerosis (MS), Parkinson's disease (PD) and stro.
In addition, the growing understanding of the gut-brain axis has also led to the development of treatments for intestinal diseases, such as inflammatory bowel disease (IBD) and irritable bowel syndrome (IB.
Summary and prospect The bidirectional communication of inflammatory signals based on the gut-brain axis is very important for regulating some normal physiological behaviors and the pathology of inflammation-related diseases, but there are still many important mechanistic questions that remain unanswered: from the afferent direction (from the Intestine to brain), intestinal immune cells can be directly recruited to the brain, but how the brain senses the initial inflammatory signal and its specific mechanism of action is unclear; while in the efferent direction (from brain to intestine), How the brain regulates intestinal inflammation is poorly understo.
The gut microbiota has now emerged as a key regulator of immune cells in the gut-brain axis, and dysbiosis has been shown to be associated with risk factors for multiple inflammatory diseases, but whether dysbiosis is responsible for this chain of events remains to be se.
unanswered questio.
Therefore, deciphering inflammatory signaling mechanisms based on the gut-brain axis is not only critical for our understanding of neural and immune communication, but also for advances in immunotherapy for gastrointestinal and neurological diseas.
Link to the original text: http://d.
org/11126/scien.
abi6087 Publisher: 11 Reprint Notice [Non-original article] The copyright of this article belongs to the author of the article, and personal sharing is welco.
Reprinting is prohibited without permissi.
The author owns all legal rights, and violators will be prosecut.
