{
  "abstract": "Multiple layers of intestinal barriers protect against uncontrolled access of gut-derived agents to the portal circulation, fuelling the liver via what is known as gut-liver axis.1 This integrated system consists of epithelial, immune and vascular compartments physiologically coordinating the absorption and distribution of nutrients. At the heart of this segmented surveillance are intestinal macrophages, specialised phagocytes organised into molecularly and anatomically distinct subsets that perform highly specialised functions dependent on their microenvironmental niche.2 Among these, a subset of macrophages closely associated with the submucosal vasculature has emerged as a critical regulator of the gut–vascular barrier (GVB). The GVB has recently been defined and characterised as the final barrier controlling access to the bloodstream, which ultimately enters the liver without further filtration.3 4 In Gut, Smets et al report that disruption of these blood vessel–associated macrophages in cirrhosis contributes to GVB dysfunction and pathological bacterial translocation5 (figure 1).",
  "authors": [
    {
      "affiliations": [
        "Vlaams Instituut voor Biotechnologie Center for Molecular Neurology, Antwerp, Flanders, Belgium"
      ],
      "name": "Sebastiaan De Schepper"
    },
    {
      "affiliations": [
        "UVCM Gastroenterology, University Bern, Bern, Switzerland"
      ],
      "name": "Reiner Wiest"
    }
  ],
  "title": "When the vascular lining loosens, dysfunctional macrophages permit pathological bacterial translocation in cirrhosis",
  "uid": "8cc04fba-722e-588e-96eb-9408e5b1362e"
}