Vagal nerve stimulation (VNS) has been shown to limit intestinal inflammation following injury, however, direct connection between vagal terminals and resident intestinal immune cells have yet to be identified. We have previously shown that enteric glia cell (EGC) expression is increased after injury through a vagal-mediated pathway to help restore gut barrier function. We hypothesize that EGCs modulate immune cell recruitment following injury and relay vagal anti-inflammatory signals to resident immune cells in the gut. EGCs were selectively ablated from an isolated segment of distal bowel with topical application of benzalkonium chloride (BAC) in male mice. Three days following BAC application, mice were subjected to an ischemia-reperfusion injury (I/R) by superior mesenteric artery occlusion for 30 minutes. VNS was performed in a separate cohort of animals. EGC⁺ and EGC^- segments were compared utilizing histology, flow cytometry, immunohistochemistry, and intestinal permeability. VNS significantly reduced immune cell recruitment after I/R injury in EGC⁺ segments with cell percentages similar to sham. VNS failed to limit immune cell recruitment in EGC^- segments. Histologic evidence of gut injury was diminished with VNS application in EGC+ segments, whereas EGC^- segments showed features of more severe injury. Intestinal permeability increased following I/R injury in both EGC⁺ and EGC^- segments. Permeability was significantly lower after VNS application compared to injury alone in EGC⁺ segments only (95.1 ± 30.0 vs. 217.6 ± 21.7 μg/mL, p<0.05). Therefore, EGC ablation uncouples the protective effects of VNS, suggesting that vagal-mediated signals are translated to effector cells through EGCs.