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. 2024 Jul;167(2):223-230.
doi: 10.1053/j.gastro.2024.03.023. Epub 2024 Mar 21.

2023 Workshop: Neuroimmune Crosstalk in the Gut - Impact on Local, Autonomic and Gut-Brain Function

Kara G Margolis  1 , Terez Shea-Donohue  2 , Diana M Cummings  2 , Patricia Greenwel  2 , Robert D Lunsford  2 , Brian D Gulbransen  3 , Isaac M Chiu  4
Affiliations

2023 Workshop: Neuroimmune Crosstalk in the Gut - Impact on Local, Autonomic and Gut-Brain Function

Kara G Margolis et al. Gastroenterology. 2024 Jul.
No abstract available

Keywords: Enteric Nervous System; Gastrointestinal; Immune System; Neuroimmune Interactions.

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Conflict of interest statement

The other authors have no conflicts to disclose.

Figures

Figure 1:
Figure 1:. Selected examples of neuroimmune interactions that modulate diverse gastrointestinal functions.
Examples noted are those discussed at the workshop. Figure 1A: (1) Gut microbiota releases products that can directly stimulate enterochromaffin (EC) cells, which release 5-HT to stimulate gut motility and pain. NKT cells also interact with EC cells via microbial lipid antigens to modulate motility; (2) Muscularis macrophages (MMs) influence GI motility by secreting bone morphogenetic protein 2 (BMP2), that activates BMP receptors (BMPR) on enteric neurons. Enteric neurons, in turn, secrete colony stimulatory factor 1 (CSF1), a growth factor required for macrophage development; (3) food allergens elicit mast cell activation of sensory neurons, resulting in pain-related and aversive behaviors; (4) Sensory neuron stimulation elicits CGRP secretion, which signals to epithelial cells (e.g, M cells, goblet cells) to induce mucus production, to increase barrier function and to provide host defense against bacterial pathogens. Figure 1B: (5) Intestinal inflammation induced by postoperative ileus signals to the NTS by way of parasympathetic/vagal afferent signaling. In turn, activation of vagal efferent nerves in the dorsal motor nucleus (DMX) stimulate cholinergic enteric neurons to secrete acetylcholine (ACh). ACh activates α7 nicotinic receptors on MMs to downregulate inflammation; (6) Stress causes adrenal release of glucocorticoids (GCs) that stimulate intestinal inflammation and dysmotility by: (a) stimulating an inflammatory subset of glia (enteric glia associated with psychological stress; eGAPS) to secrete CSF1, inducing monocyte secretion of TNFa, resulting and (b) causing transcriptional immaturity in enteric neurons, acetylcholine deficiency, and dysmotility via TGF-β2.
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