A gut-vascular barrier controls the systemic dissemination of bacteria

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Science  13 Nov 2015:
Vol. 350, Issue 6262, pp. 830-834
DOI: 10.1126/science.aad0135

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A gut bacterial containment system

Trillions of bacteria selectively inhabit our guts, but how do our bodies keep them contained? Spadoni et al. describe a “gut-vascular barrier” that prevents intestinal microbes from accessing the liver and the bloodstream in mice (see the Perspective by Bouziat and Jabri). Studies with human samples and in mice revealed that the cell biology of the gut-vascular barrier shares similarities with the blood-brain barrier of the central nervous system. Pathogenic bacteria such as Salmonella typhimurium could penetrate the gut-vascular barrier in mice, gaining access to the liver and bloodstream, in a manner dependent on the Salmonella pathogenicity island 2–type III secretion system.

Science, this issue p. 830; see also p. 742


In healthy individuals, the intestinal microbiota cannot access the liver, spleen, or other peripheral tissues. Some pathogenic bacteria can reach these sites, however, and can induce a systemic immune response. How such compartmentalization is achieved is unknown. We identify a gut-vascular barrier (GVB) in mice and humans that controls the translocation of antigens into the blood stream and prohibits entry of the microbiota. Salmonella typhimurium can penetrate the GVB in a manner dependent on its pathogenicity island (Spi) 2–encoded type III secretion system and on decreased β-catenin–dependent signaling in gut endothelial cells. The GVB is modified in celiac disease patients with elevated serum transaminases, which indicates that GVB dismantling may be responsible for liver damage in these patients. Understanding the GVB may provide new insights into the regulation of the gut-liver axis.

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