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Extracellular vesicles (EVs) serve as pivotal mediators of inter\u2010organ communication. Here, this study demonstrates that circulating EVs from colitis exacerbate colitis severity by inducing neutrophil extracellular trap (NET) formation. Inhibition of circulating EV secretion or NET formation alleviates colitis severity. Mechanistically, EVs enriched with interleukin\u20107 receptor (IL\u20107R) are identified as critical drivers of NET\u2010mediated colitis exacerbation. Downregulation of IL\u20107R ameliorates colitis symptoms, whereas IL\u20107R upregulation worsens disease progression. IL\u20107R is found to induce NETs via the protein\u2010arginine deiminase type 4 (PAD4) pathway to aggravate colitis. Furthermore, this study establishes that thymus\u2010derived EVs are the primary source of IL\u20107R\u2010enriched circulating EVs. 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