Lipopolysaccharide Induces Cell Death in Cultured Porcine Myenteric Neurons

Infiltration of Mast Cells in Rat Colon Is a Consequence of Ischemia/Reperfusion

“…This since enteric neuronal VIP expression is upregulated in several pathophysiological situations, such as blockade of axonal transport or axotomy [24], intestinal hypertrophy [25], or ischemia [9], and in patients with Crohn's disease [34]. Furthermore, in vitro studies, e.g., primary culture of myenteric neurons from porcine or rat small and large intestine, show that the proportion of neurons expressing VIP markedly increases compared to in vivo [23,[35][36][37]. Addition of VIP to cultured rat small intestine myenteric neurons promotes neuronal survival [35,36] and recently it was shown that VIP, when added to cultured myenteric neurons from rat small intestine in combination with lipopolysaccharide (LPS), markedly reduces LPS-induced neuronal cell death [38].…”

“…Furthermore, in vitro studies, e.g., primary culture of myenteric neurons from porcine or rat small and large intestine, show that the proportion of neurons expressing VIP markedly increases compared to in vivo [23,[35][36][37]. Addition of VIP to cultured rat small intestine myenteric neurons promotes neuronal survival [35,36] and recently it was shown that VIP, when added to cultured myenteric neurons from rat small intestine in combination with lipopolysaccharide (LPS), markedly reduces LPS-induced neuronal cell death [38]. The present study show an increased number of myenteric neurons expressing VIP from days 1 to 3 postoperatively in both sham and I/R segments and the VIP upregulation is therefore suggested to be due to the surgical procedures.…”

The effects of glucagon-like peptide 2 on enteric neurons in intestinal inflammation

“…However, it is also a potent regulator of the mucosal inflammatory response, acting to shift an acute T helper 1 (Th1) inflammatory response of the lamina propria to a healing milieu characterized by an increase in insulin‐like growth factor‐1 production by resident macrophages 17 . In these studies, it was noted that GLP‐2 treatment appeared to improve all aspects of the morphology of the inflamed mucosa; given that GLP‐2 induces the production of VIP by neurons of the submucosa and that VIP has been shown to be protective for enteric neurons, 18–20 we hypothesized that GLP‐2 would be protective to the ENS in models of mucosal inflammation. To test this, we induced colitis using trinitrobenzene sulfonic acid (TNBS), and examined the effects of GLP‐2 therapy on mucosal markers of inflammation, the number of neurons per ganglion in the submucosal plexus, the proportional expression of different neuronal subtypes and the number of associated enteric glial cells.…”

Galectin-3 causes enteric neuronal loss in mice after left sided permanent middle cerebral artery occlusion, a model of stroke

“…Together our data strongly suggest that focal ischemic stroke causes enteric neuronal loss, in parallel with central manifestations, and that the neuroimmune mechanism behind involves gal-3 and TLR4 receptor activation. This may explain the graded and extended (involving both submucous and myenteric neurons) neuronal susceptibility to pMCAO observed in vivo , as immunocytochemical analyses show that TLR4 is more abundantly expressed in the distal, compared to the proximal, bowel in both neurons and glia cells2627. Astrocytes mediate a neurotoxic inflammatory response in the central nervous system through TLR4 activation causing oxidative stress28.…”