TY - JOUR
T1 - A gut-vascular barrier controls the systemic dissemination of bacteria
AU - Spadoni, Ilaria
AU - Zagato, Elena
AU - Bertocchi, Alice
AU - Paolinelli, Roberta
AU - Hot, Edina
AU - Di Sabatino, Antonio
AU - Caprioli, Flavio
AU - Bottiglieri, Luca
AU - Oldani, Amanda
AU - Viale, Giuseppe
AU - Penna, Giuseppe
AU - Dejana, Elisabetta
AU - Rescigno, Maria
PY - 2015/11/13
Y1 - 2015/11/13
N2 - 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 bloodstream 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.
AB - 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 bloodstream 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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U2 - 10.1126/science.aad0135
DO - 10.1126/science.aad0135
M3 - Article
C2 - 26564856
AN - SCOPUS:84946926173
VL - 350
SP - 830
EP - 834
JO - Science
JF - Science
SN - 0036-8075
IS - 6262
ER -