Abstract
Intestinal immunity is finely regulated by several concomitant and overlapping mechanisms, in order to efficiently sense external stimuli and mount an adequate response of either tolerance or defense. In this context, a complex interplay between immune and nonimmune cells is responsible for the maintenance of normal homeostasis. However, in certain conditions, the disruption of such an intricate network may result in intestinal inflammation, including inflammatory bowel disease (IBD). IBD is believed to result from a combination of genetic and environmental factors acting in concert with an inappropriate immune response, which in turn interacts with nonimmune cells, including nervous system components. Currently, evidence shows that the interaction between the immune and the nervous system is bidirectional and plays a critical role in the regulation of intestinal inflammation. Recently, the maintenance of intestinal homeostasis has been shown to be under the reciprocal control of the microbiota by immune mechanisms, whereas intestinal microorganisms can modulate mucosal immunity. Therefore, in addition to presenting the mechanisms underlying the interaction between immune and nervous systems in the gut, here we discuss the role of the microbiota also in the regulation of neuroimmune crosstalk involved in intestinal homeostasis and inflammation, with potential implications to IBD pathogenesis.
Highlights
The enteric nervous system (ENS) constitutes a major autonomic division of the nervous system that provides the intrinsic innervation of the gut, capable of controlling different functions, such as motility, mucosal secretion and absorption, mucosal growth, local blood flow, and the immune function [1]
GSNO was shown to be able to restore mucosal barrier function in Crohn’s disease (CD) colonic mucosal specimens [124]. In another experimental study focused on enteric glial cells (EGC), Zhang et al revealed that glial-derived neurotrophic factor (GDNF), another molecule released by EGC, could regulate the integrity of the intestinal barrier
PAR1-mediated Cl− secretion might occur by activation of the receptor on the submucosal secretomotor neurons; PAR2-mediated Cl− secretion might occur by activation of the receptor on the epithelial cells
Summary
The enteric nervous system (ENS) constitutes a major autonomic division of the nervous system that provides the intrinsic innervation of the gut, capable of controlling different functions, such as motility, mucosal secretion and absorption, mucosal growth, local blood flow, and the immune function [1]. The ENS consists of two interconnected networks of ganglia and fibers encircling the GI tract, arranged in a peculiar way, which confers the ability to mediate its own reflexes. In this context, evidence shows that ENS can work independently of the CNS [3]. Despite the ability of the ENS to regulate motility and secretion in an autonomous way, there are many connective links with the CNS, working in a bidirectional fashion [4]. The communication between the ENS and the immune system within the mucosa participates in the Mediators of Inflammation control of major GI functions but can be associated with pathological conditions, such as inflammatory bowel disease (IBD)
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