Inflammatory bowel disease( IBD ) flares are made worse by psychological stress. Schneider et al., in Cell demonstrate that glucocorticoids stimulate inflammation mediated by neurons and glia in the enteric nervous system. Restraint or social stress increase colon inflammation in a mouse model of colitis caused by either dextran sodium sulfate( DSS ) or lack of IL-10. For the stress-induced aggravation of colitis, monocytes and TNF are necessary but not adaptive immune cells, innate lymphoid cells or IL-6. Stress-induced corticosteroids mediate colitis by signaling in enteric glia and neurons, but not in myeloid or epithelial cells, in contrast to catecholamines that are protective. An inflammatory subset of the Nur + Ripk1 + Stat3 + glia, which express Csf1, is induced by stress and the glucocorticoid receptor agonist dexamethasone. This glia subset, or CSF1 blockade, is deleted to confer resistance to stress-induced colitis. Additionally, stress and dexamethasone increase the proportion of immature Tgfb2 + neurons while decreasing the number of nNOS + and ChAT + mature neurons. TGF2 blockade restores neuron maturation, whereas nicotine supplementation reverses stress-induced dysmotility in DSS colitis mice but not CSF1 or TNF neutralization. Stressful lifestyles are linked to more severe IBD, increased TNF production, higher TGFB2 expression, and transcripts connected to monocyte recruitment and inflammation in humans.Access the preview of subscription content here by going to your institution.options for access