Abstract
Inflammatory bowel disease, irritable bowel syndrome and severe central nervous system injury can lead to intestinal mucosal barrier damage, which can cause endotoxin/enterobacteria translocation to induce infection and is closely related to the progression of metabolic diseases, cardiovascular and cerebrovascular diseases, tumors and other diseases. Hence, repairing the intestinal barrier represents a potential therapeutic target for many diseases. Enteral afferent nerves, efferent nerves and the intrinsic enteric nervous system (ENS) play key roles in regulating intestinal physiological homeostasis and coping with acute stress. Furthermore, innervation actively regulates immunity and induces inherent and adaptive immune responses through complex processes, such as secreting neurotransmitters or hormones and regulating their corresponding receptors. In addition, intestinal microorganisms and their metabolites play a regulatory role in the intestinal mucosal barrier. This paper primarily discusses the interactions between norepinephrine and β-adrenergic receptors, cholinergic anti-inflammatory pathways, nociceptive receptors, complex ENS networks, gut microbes and various immune cells with their secreted cytokines to summarize the key roles in regulating intestinal inflammation and improving mucosal barrier function.
Highlights
Function of the digestive tract is controlled by both CNS and enteric nervous system (ENS), and it is one of the most extensive immune organs in the body, maintaining the balance between immunogenicity and immune tolerance of food, foreign bodies and microorganisms
This paper focuses on the crosstalk between Autonomic nervous system (ANS), afferent nerve and ENS and the immune impact on Intestinal epithelial cells (IECs), as well as their protecting role in intestinal mucosal barrier
Stanley et al found that in gastrointestinal disorders associated with stroke, due to a loss of ileal cholinergic Choline acetyltransferase (ChAT)+ neurons, which stimulate the development of proinflammatory immunity, increased barrier permeability led to intestinal bacterial translocation and secondary infection (Stanley et al, 2016)
Summary
Function of the digestive tract is controlled by both CNS and ENS, and it is one of the most extensive immune organs in the body, maintaining the balance between immunogenicity and immune tolerance of food, foreign bodies and microorganisms. Stanley et al found that in gastrointestinal disorders associated with stroke, due to a loss of ileal cholinergic ChAT+ neurons, which stimulate the development of proinflammatory immunity, increased barrier permeability led to intestinal bacterial translocation and secondary infection (Stanley et al, 2016) (see Table 4).
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