In fact, by using an animal model of colitis induced by rectal administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS), the authors demonstrated that oxytocin and S in combination attenuated intestinal inflammation by decreasing inflammatory infiltrates into the colon and by affecting the colon expression of TNF-α and IFN-γ; moreover, oxytocin and S co-administration prevented the transmission of inflammation-evoked signals to paraventricular nucleus, amygdala, and piriform cortex [117]. Here, OXT is linked to colitis.