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Here, we show that mesenteric macrophage\u2013monocyte interactions limit systemic infection during Salmonella Typhimurium (STm)\u2013induced gut inflammation. Using Ccr2-deficient mice and fate-mapping approaches, we identified two distinct granulocyte-monocyte progenitor (GMP)-derived macrophage populations in the gut mesentery, LYVE1hi TIM4(\u2212) and LYVE1lo\/\u2212 TIM4(\u2212) subsets, alongside embryonically derived LYVE1hi TIM4(+) macrophages. LYVE1lo\/\u2212 TIM4(\u2212) macrophages, but not LYVE1hi macrophages, removed excessively recruited neutrophils during STm infection, whereas newly mesentery-recruited monocytes were the primary source of inflammatory cytokines. Moreover, depletion of mesentery-resident macrophages in mice lacking Csf1 in serous stromal cells resulted in excessive recruitment of GMP-derived monocytes accompanied by elevated expression of inflammatory cytokines, thereby accelerating mortality during STm infection. Together, our findings reveal that the mesenteric macrophage\u2013monocyte circuit buffers the escalation of gut infection into systemic inflammation.<\/jats:p>","DOI":"10.1084\/jem.20251492","type":"journal-article","created":{"date-parts":[[2026,3,25]],"date-time":"2026-03-25T06:21:06Z","timestamp":1774419666000},"update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":1,"title":["Mesenteric macrophage-monocyte circuit controls systemic inflammation during enteric bacterial infection"],"prefix":"10.1084","volume":"223","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5367-2148","authenticated-orcid":true,"given":"Jiseon","family":"Kim","sequence":"first","affiliation":[{"name":"University of Illinois College of Medicine 1 Department of Pharmacology and Regenerative Medicine, , Chicago, IL,","place":["USA"]},{"name":"Center for Lung and Vascular Biology, University of Illinois College of Medicine 2 , Chicago, 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