Vagotomy ameliorates colitis [68] Variable outcomes of nicotinic agonists on the course of colitis [51] Vagal nerve stimulation ameliorates intestinal inflammation: Postoperative ileus, [69] septic ileus Intestinal barrier breakdown [70] Mast cell activation [28] Ischemia reperfusion injury
Dopamine, adrenaline, and noradrenaline
Dopamine receptors, adrenergic receptors a and b
CNS neurons Recruited immune cells Postganglionic Nerves throughout the GI tract
Potent inhibitor of Th1 and macrophage functions Multiple effects on cytokine and chemokine secretion (reviewed a.o. in [30, 32, 71]) In APCs an decrease of IL-12 Type 1, proinflammatory TNF-a Type 1, proinflammatory IFN-g Type 1, proinflammatory IL-2 Type 1 IL-1 Proinflammatory IL-4 Type 2, anti-inflammatory IL-3 Hemopoietic factor GM-Hemopoietic factor CSF MIP-1-Proinflammatory chemokine In APCs an increase of IL-10 Type 2, anti-inflammatory TGF-a Type 2, anti-inflammatory IL-8 Proinflammatory Chemotactic for neutrophils, macrophages, and T lymphocytes [72] Promotes the development of the precursors of granulocytes and macrophages [73]
Vasoactive intestinal peptide
VPAC1 VPAC2
Recruited immune cells Enteric nerve plexus Lamina propria nerves CNS
Amelioration of TNBS-induced colitis by shifting T-cell responses from Th1 to Th2 [74]. Generation of tolerogenic dendritic cells [75]
Substance P
NK-1R NK-2R NK-3R
Recruited immune cells, lamina propria macrophages, colonic glia Motor neurons of intestinal muscularis Lamina propria nerves CNS
Antagonists ameliorate disease in a rat model of TNBS-induced colitis [76] NK-1R−/− mice protected from inflammatory diarrhoea in C. difficile toxin A [77] Proinflammatory activation of myeloid cells
Neuropeptide Y Peptide YY Pancreatic polypeptide
6 Y receptors (Y1-6R)
CNS Mononuclear blood leukocytes T cells, APCs
Enhanced T-cell cytokine release Reduced APC cytokine release and function [78, 79]
